Scurvy, or hypovitaminosis C, is caused by prolonged and severe deficiency of ascorbic acid.¹ Cutaneous manifestations include follicular hyperkeratosis, perifollicular petechiae, corkscrew hair, and ecchymosis.¹ Inaccurately believed to be of historical interest, this disease remains current and relevant. Scurvy has been reported in patients with substance abuse,² cirrhosis,² AIDS,³ metastatic cancer,⁴ peritoneal dialysis⁵, liver transplant,⁶ cerebral palsy,⁷ autism,⁸ schizophrenia,⁹ anorexia nervosa,¹⁰ depression,¹¹ food faddism,¹² and food allergy.¹³

Humans cannot synthetize ascorbic acid de novo, and must rely on dietary sources of vitamin C, which include fruits and vegetables. Potatoes, tomatoes, berries, citrus, and green vegetables are particularly rich in vitamin C. Inadequate vitamin C intake is the most common cause of scurvy. Increased vitamin C loss may be seen in patients with peritoneal dialysis.5 It is a water-soluble vitamin and depletion of body stores only takes one to three months.

Vitamin C acts as an antioxidant and a cofactor in several processes, which include prostaglandin metabolism, fatty acid transport, norepinephrine synthesis, and collagen biosynthesis. Vitamin C is required as a reducing cofactor for prolyl hydroxylase in order to convert proline to hydroxyproline on procollagen. Inappropriate collagen biosynthesis is the basis for many cutaneous manifestations of scurvy.

CLINICAL CASE

We report a case of a 59-year-old homeless man presenting to the emergency department in a state of alcoholic intoxication, with icterus, ascites, and lower extremity petechiae (Figure 1). He had no relevant known past medical history and was taking no medication. He admitted to active alcohol abuse but did not consume other drugs. Our dermatology service was consulted to rule out vasculitis in this patient. Physical examination revealed icterus, extremely poor dental hygiene, and lower extremity perifollicular petechiae with follicular hyperkeratosis. Complete blood count revealed normocytic normochromic anemia and a platelet count within normal limits. Coagulation studies revealed a prolonged INR of 2.0. On the basis of a clinical suspicion of scurvy, serum ascorbic acid levels were ordered and a skin biopsy was performed. Skin biopsy revealed dystrophic hair and perifollicular hemorrhage, with absence of vasculitis (Figure 2). A Turnbull Blue stain further highlighted the extent of hemosiderin deposition (Figure 3). Scurvy was diagnosed. The patient suffered from concurrent alcoholic cirrhosis, which explained his prolonged INR. Ascorbic acid repletion was performed immediately. Ascorbic acid 200 mg po daily was prescribed, as multivitamins only contain about 60 mg of ascorbic acid. Serum vitamin C levels were 14 mg/L. Levels are considered deficient when below 75 mg/L. The skin biopsy result was available 14 days prior to the lab results and allowed for earlier appropriate therapy. Cutaneous lesions eventually healed completely.

CONCLUSION

The differential diagnosis of lower extremity petechiae is wide. In appropriate patient populations, clinicians must keep a high index of suspicion to diagnose scurvy. Follicular hyperkeratosis, perifollicular petechiae, corkscrew hair, ecchymosis and dental disease are further clues to establishing diagnosis. Skin biopsy is a helpful diagnostic tool and may allow even faster diagnosis than dosing serum ascorbic acid levels.

Dr. Vincent Richer has no financial interests to disclose.

Dr. Richer is a PGY-4 Dermatology Resident. He is Chief Resident at the Université de Montréal in Quebec, Canada.

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