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Gut. 2007 November; 56(11): 1535.
PMCID: PMC2095658



From question on page 1511

The clinical and endoscopic findings together with a re‐evaluation of dietary recall, showing an absence of dietary vitamin C sources, suggested a diagnosis of scurvy. An ascorbic acid assay yielded no detectable amounts (<0.12 mg/dl, normal range 0.2–1.9 mg/dl). The patient was treated for 2 weeks with a daily oral dose of 200 mg vitamin C and a balanced diet including daily consumption of fruit. In the following week a prompt resolution of all symptoms was observed and a normal vitamin C level (1.1 mg/dl) was achieved after 5 days of therapy.

Clinical manifestation of scurvy reflects the role that vitamin C plays in collagen synthesis. Ascorbate is a cofactor for prolyl and lysyl hydroxylases in the biosynthesis of collagen. The characteristic tissue and capillary fragility of scurvy has been attributed to a defect in the praline hydroxylation step of collagen biosynthesis.1,2 Nowadays, scurvy reports are rarer and less common in children, except in underdeveloped countries and in some “at risk” categories, including persons with neurological or behavioural disorders, anorexia and intestinal malabsorption.3 It is important for the gastroenterologist to include scurvy in the differential diagnosis of patients presenting with purpuric lesions (also at gastric mucosa levels), joint pain and bleeding gums, because appropriate diagnosis and treatment is life saving, even when patients present in the most advanced stages.


1. Pimentel L. Scurvy: historical review and current diagnostic approach. Am J Emerg Med 2003. 21328–332.332 [PubMed]
2. Levine M. New concepts in the biology and biochemistry of ascorbic acid. N Engl J Med 1986. 314892–902.902 [PubMed]
3. Rajakumar K. Infantile scurvy: a historical perspective. Pediatrics 2001. 108E76–E78.E78 [PubMed]

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