Scurvy in an alcohol-dependent patient with a severely unbalanced diet
Scurvy occurs due to vitamin C deficiency.1, 2 Vitamin C is a factor necessary in collagen synthesis in skin and connective tissue. Its deficiency results in fragility of capillaries and surrounding tissue. The clinical symptoms in the initial stage are malaise and easy fatigability. Other symptoms gradually develop, including easy bruising, petechiae, perifollicular petechiae, edema, anemia, periodontal disease, myalgia, and corkscrew hairs. In the late stage, generalized edema, severe jaundice, and acute spontaneous bleeding occur. Scurvy is treated by vitamin C supplementation and improves rapidly after treatment. This report describes an alcohol-dependent patient who developed scurvy due to a severely unbalanced diet. The patient provided written consent to publish this report.
The patient was a 45-year-old man with alcohol dependency. He presented to the emergency outpatient clinic with chief complaints of easy fatigability, loss of appetite, and pain in bilateral lower legs. He had tended to drink too much alcohol since his twenties. Although he had alcoholic liver injury, he would not stop alcohol ingestion. For the past several years, he had been drinking approximately 1500 mL of beer and 350 mL of whisky per day. He had a severely unbalanced diet. He ate only ready-made meals that contained some meats, instant food from convenience stores, and seldom any fresh vegetables or fruits. He had easy fatigability and loss of appetite from 3 weeks before presentation to the clinic. He gradually became unable to consume anything but water. At the same time, he developed pain in bilateral lower legs and had difficulty in ambulation.
His vital signs were normal on presentation to the clinic. Gingival swelling and lower leg purpura and edema were observed. A blood test showed macrocytic anemia (hemoglobin 5.8 g/dL, mean corpuscular volume 108 μm3). The platelet count and coagulation profile were normal. Vitamin B12 was within normal limits but serum folic acid was low at 1.3 ng/mL (normal range: 2.4–12.0). Vitamin C was very low at <0.2 μg/mL (normal range: 5.5–16.8). The patient was diagnosed with scurvy based on clinical presentation, unbalanced diet, and abnormally low vitamin C. During hospitalization, the patient was treated for scurvy using oral vitamin C (1200 mg/day) and for megaloblastic anemia using oral folic acid (15 mg/day). Approximately 3 weeks later, his symptoms were improved and vitamin C and folic acid administration were discontinued. The patient was monitored for approximately 2 weeks, and he had no recurrence of symptoms and was discharged from the hospital.
In modern society, scurvy is rarely seen due to improved food supplies. However, modern cases of scurvy have been reported in alcohol-dependent patients, patients with mental disorders, people with severe food allergies, patients with eating disorders, and hemodialysis patients.1 The patient in this study had a severely unbalanced diet that contained some meats but hardly any vegetables or fruits. Vitamin B1 in meats may have prevented him from developing Wernicke's encephalopathy, but the lack of Vitamin C due to insufficient vegetables and fruits may have caused scurvy. As alcohol-dependent patients, such as the patient in this study, often have an unbalanced diet for a long time and alcohol inhibits vitamin C absorption,3 it is necessary to be mindful of scurvy in alcohol-dependent patients.
