To the Editor:
A 28-year-old recently homeless white man with a history of heroin abuse was admitted with a worsening rash and left ankle pain of 1 week’s duration, as well as subjective fever after 3 weeks of a productive cough, sore throat, hoarse voice, and general malaise. Six days prior to presentation, he developed redness and swelling of the dorsal aspects of both hands with accompanying rash, and 2 days prior to presentation he developed a similar rash on the legs with associated left ankle pain, redness, and swelling. He also reported eye redness, pain, photophobia, crusty eye discharge, and a pins and needles sensation on the soles of both feet. Additionally, he had noted difficulty with urination over several days. He had been homeless for less than 1 month prior to admission.
On physical examination, the patient appeared to be well nourished. Skin examination was notable for scattered perifollicular hemorrhagic and hyperkeratotic papules ranging in size from 3 to 6 mm with associated nummular alopecia of the bilateral medial thighs (Figure); well-demarcated desquamated patches on the weight-bearing aspects of the plantar feet; and a 2.0-cm, well-demarcated, thinly raised erythematous patch of the inferolateral penile shaft. Oral examination was notable for multiple discrete areas of ulceration on the lateral aspects of the tongue. Ophthalmic examination revealed conjunctival injection and photophobia. The ankles were edematous and tender (the left ankle more than the right), and range of passive motion was limited by pain.
Laboratory values were remarkable for a hemoglobin count of 13.1 g/dL (reference range, 14.2–18 g/dL), erythrocyte sedimentation rate of 31 mm/h (reference range, 0–10 mm/h), and C-reactive protein level of 5.4 mg/dL (reference range, 0–0.8 mg/dL). Urinalysis was unremarkable, blood cultures were negative, and a chest radiograph was normal. Human immunodeficiency virus and rapid plasma reagin tests were negative, with normal levels of IgG, IgA, and IgM. IgE was elevated at 572 IU/mL (reference range, 0–100 IU/mL). Ultrasonography of the leg was negative for deep vein thrombosis, and a left ankle radiograph was negative for fracture. The patient previously was found to have antinuclear antibodies of 1:40 and negative antineutrophil cytoplasmic antibodies, anti–double-stranded DNA, anti–Sjögren syndrome antigens A and B, and cryoglobulins, as well as normal complement levels. The constellation of rash, arthritis, conjunctivitis, and difficulty with urination raised a high suspicion for reactive arthritis; however, the patient was found to be HLA-B27 negative with a negative urine chlamydia test.
The patient was mildly hypokalemic at 2.9 mmol/L (reference range, 3.5–5.0 mmol/L) and hypoalbuminemic at 3.6 g/dL (reference range, 3.9–5.0 g/dL). He had a slightly elevated international normalized ratio of 1.4 (reference range, 0.9–1.2). Further questioning revealed that his diet consisted mostly of soda and energy drinks; his vitamin C level was subsequently checked and found to be 0 mg/dL (reference range, 0.2–2.0 mg/dL). A diagnosis of scurvy was made, and his symptoms improved at the hospital while maintaining a diet with normal levels of vitamin C. His rash had markedly improved by hospital day 2, joint swelling decreased, and the conjunctival injection and eye pain had resolved. Upon outpatient follow-up, his rash and joint swelling continued to improve, and he had not experienced any further areas of hair loss.
Scurvy, a condition caused by vitamin C deficiency, is a disease of historical importance, as it ravaged ships full of sailors in days past; however, its incidence has decreased drastically since Lind1 first described its treatment using citrus fruits in 1753. Nonetheless, even with modern day access to foods rich in vitamin C, scurvy is far more common than expected in the developed world.
Vitamin C (ascorbic acid) plays a crucial role in human biochemistry. Although many plants and animals can synthesize ascorbic acid, humans and other animals such as guinea pigs lack the required enzyme, making vitamin C an essential nutrient required in dietary intake.2-4 Hypovitaminosis C leads to scurvy when collagen production becomes impaired due to lack of ascorbic acid as a required cofactor for its synthesis, which leads to tissue and capillary fragility, causing hemorrhage and perivascular edema.4 The diagnosis of scurvy is clinical and typically is based on signs such as perivascular hemorrhage, bleeding gums, anemia, impaired wound healing, and ecchymoses in the setting of vitamin C deficiency (<11 μmol/L or <0.2 mg/dL) with rapid resolution upon vitamin C supplementation.5