A 65-year-old man with a history of alcohol and tobacco use and few medical interactions presented with 1 week of progressive dyspnea. Examination revealed a cachectic man with large areas of nonpainful ecchymoses on the posterior thighs (Figure). Additional skin findings included spider angiomata on the face and chest, scattered bruising on upper extremities, and diffuse perifollicular purpura on lower extremities. Labs revealed normocytic anemia and thrombocytopenia with a low reticulocyte index. Hemolysis labs and peripheral smear were unremarkable. Iron studies, fibrinogen levels, and platelet function studies were within normal limits. Computed tomography scans (head, chest, abdomen/pelvis), upper gastrointestinal endoscopy, and colonoscopy revealed no clear sources of bleeding.
The patient was malnourished, with hypoalbuminemia 2.7 g/dL (N 3.4-5 g/dL). Upon further questioning, he reported daily consumption of 12 beers for several decades and a diet consisting mainly of canned foods. A presumptive diagnosis of vitamin C deficiency was made, and empiric 1 g intramuscular vitamin C was administered. Ecchymoses and purpura improved within 3 days. Labs drawn prior to initiation of treatment subsequently confirmed a deficiency in vitamin C with levels <0.1 mg/dL (N 0.2-2 mg/dL) as well as vitamin A, vitamin D, zinc, and folate deficiencies. Vitamin E, B12, copper, and selenium were normal. On discharge, the patient was provided with multivitamin and mineral supplements.
Considered a historical disease associated with sailors and famines, scurvy is a rare diagnosis in the developed world due to wide availability of fortified foods. In the United States, scurvy largely occurs in severely malnourished individuals, drug/alcohol users, those with eating disorders, and patients with underlying disorders (eg, ulcerative colitis). Scurvy is the clinical manifestation of vitamin C deficiency and occurs when plasma levels are <0.2 mg/dL. Symptoms develop by the third month of insufficient intake.1
Vitamin C plays an important role in the hydroxylation of proline and lysine residues during collagen synthesis. Abnormal collagen affects blood vessel integrity leading to fragile capillaries, perivascular edema, and red cell leakage. Common findings include perifollicular hemorrhage, “corkscrew” hairs, ecchymoses, gingivitis, arthralgias, impaired wound healing, and anemia.2 Treatment is daily 300-1000 mg replacement for 1 month. Of note, a daily multivitamin with a minimum of 100 mg thiamine, 2 mg vitamin B6, and 400 µg-1 mg folic acid is recommended for adults with alcohol abuse disorder. Interestingly, these recommendations do not include supplementation with vitamin C.3
Our goal in reporting this case is to provide the context for a modern case of scurvy, as pathology resulting in hospitalization from nutritional deficiencies are rare in developed nations and can be easily missed. As our case demonstrates, they should be considered especially in patients with a history of heavy drinking. Alcohol use disorders are very common in the United States, with an estimated 18% lifetime prevalence of abuse in the general population. Additionally, 1 in 4 patients admitted to hospitals have alcohol-related issues.4 Electrolyte abnormalities are well described in patients with alcohol abuse, whereas nutritional deficiencies often remain undiagnosed.5 Therefore, individuals at risk for malnutrition should be screened for multiple deficiencies and promptly treated. This is especially true for scurvy, as lack of treatment can be deadly.
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-Audrey W. Jiang, MD candidate, Mahima Vijayaraghavan, MD, MBA, Elliot G. Mills, MD, Anthony R. Prisco, MD, PhD, Joseph R. Thurn, MD, MPH
This article originally appeared in the May issue of The American Journal of Medicine.
