Scurvy is a rare form of hypovitaminosis which can manifest in various ways. Scurvy caused by a lack of vitamin C impairs collagen production, leading to disruption in the structure of capillaries, as well as to the appearance of petechiae, purpura and ecchymosis. It can also cause bleeding and hypertrophy of the gums, as well as intra-articular bleeding, arthralgia, myalgia and limited joint movement. It also causes anemia, pulmonary hypertension and inf lammation, as well as impairing prostaglandin metabolism and increasing inflammatory markers.[2] Scurvy is a rare disease which does not usually come to mind in medical practice. It causes complications and hemorrhages that can lead to death if left untreated. It can also be confused with many other diseases and plays a mimetic role.[3]

In this article, we present a case of scurvy in a 50-year-old male prisoner and emphasize the importance of adequate nutritional provision and routine monitoring in institutionalized settings.

Figure 1. Gingival hypertrophy.

Figure 2. Ecchymoses in both lower extremities.

Table 1: Laboratory results of the patient

Tissue transglutaminase antibody (immunoglobulin (Ig) A and Ig G) was negative, procalcitonin was 0.2 ng/mL, factor 7 and factor 13 level was normal. Urine analysis was negative for protein, erythrocytes and leukocytes. Antinuclear antibody was negative, antiphospholipid antibodies, rheumatoid factor, antineutrophil cytoplasmic antibodies and cryoglobulins were negative.

Chest radiography and echocardiographic findings were all normal. Abdominal ultrasonography was also normal, and there was no splenomegaly. Bilateral X-ray radiographs of the lower extremities were normal. Lower extremity computed angiography and Doppler ultrasonography revealed no vascular pathology. Infection, malignancy and vasculitis were excluded, as C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR) were elevated on admission. There was no low platelet count and factor deficiency that could cause bleeding. Vitamin C level (ascorbic acid) was 0.1 mg/dL (reference range: 0.4 to 2.1 mg/dL). Skin biopsy revealed perifollicular hemorrhage.

Based on the patient's history of malnutrition, the presence of clinical findings such as gingival hypertrophy and bleeding, and the evaluation of laboratory and biopsy results, a rare scurvy was diagnosed. In addition, B12 and folate deficiency was thought to be secondary to nutritional deficiency. The patient was initiated on ascorbic acid 500 mg/day b.i.d. After one week, 500 mg/day was prescribed. At the end of two weeks, clinical complaints decreased and hemorrhagic lesions in the legs regressed almost completely (Figure 3). Written informed consent was obtained from the patient.

Figure 3. Complete disappearance of bleeding signs after treatment.

The rare nature of the disease and the non-specific clinical presentation can lead to a delay in diagnosis after a thorough diagnostic workup, often including radiological imaging.[5,6]

Case reports in the literature suggest that patients are frequently misdiagnosed with hematological, rheumatological, autoimmune or bone diseases, as well as infectious diseases such as deep vein thrombosis, meningitis, meningococcal infection or syphilis.[7] In a study by Amogne et al.[8] in a prison in Ethiopia, 118 prisoners had leg pain, swelling, petechiae, oral lesions, severe anemia (<6 g/dL), leukopenia and elevated acute phases and were treated for deep vein thrombosis, arthritis, sexually transmitted disease or vasculitis, but later found that this was due to vitamin C deficiency. In a study conducted by Bennett and Coninx,[9] in prisoners in East Africa, a previously undiagnosed disease called “wooden leg” by local people, which did not respond to various treatments and usually manifested as edema and stiffness in the lower extremities, attracted attention. In the evaluations of these prisoners, serum ascorbic acid levels were found to be significantly low and scurvy was diagnosed based on these findings. A significant improvement in clinical symptoms was observed with oral ascorbic acid treatment. In addition, these individuals had inadequate dietary habits in terms of vitamin C. These findings suggest that scurvy is a diagnosis that should not be ignored even today in communities where malnutrition is widespread. Our case had a clinic similar to those in the literature, with leukopenia, severe anemia and acute phase elevation. This case has prompted clinicians to perform extensive further investigations to explain the present clinic. Our study is an exemplary study which would contribute to the literature and may be an example for early diagnosis of diseases related to easy-to-treat nutritional deficiencies such as scurvy by taking a good anamnesis about nutrition and making anthropometric measurements, especially in prisoner patients.

In conclusion, scurvy is rarely seen due to inadequate ascorbic acid intake currently. The rarity of the disease, its clinical features affecting many systems, and its ability to mimic diseases such as vasculitis may cause delays in diagnosis, thereby leading the clinician to perform further investigations, which results in increased financial burden. It is of utmost importance for clinicians to consider scurvy, which can lead to serious consequences, in the differential diagnosis of patients presenting with bleeding symptoms and at risk of malnutrition, such as prisoners.

Data Sharing Statement: The data that support the findings of this study are available from the corresponding author upon reasonable request.

Author Contributions: Conceptualization, methodology, writing, review and editing, supervision, writing-original draft: K.I., O.C.; Data curation: K.I. All authors have read and agreed to the published version of the case report.

Conflict of Interest: The authors declared no conflicts of interest with respect to the authorship and/or publication of this article.

Funding: The authors received no financial support for the research and/or authorship of this article.

1) Doseděl M, Jirkovský E, Macáková K, Krčmová LK, Javorská L, Pourová J, et al. Vitamin C-Sources, physiological role, kinetics, deficiency, use, toxicity, and determination. Nutrients 2021;13:615. doi: 10.3390/nu13020615.

2) Golder JE, Bauer JD, Barker LA, Lemoh CN, Gibson SJ, Davidson ZE. Prevalence, risk factors, and clinical outcomes of vitamin C deficiency in adult hospitalized patients in high-income countries: A scoping review. Nutr Rev 2024;82:1605-21. doi: 10.1093/nutrit/nuad157.

3) Kassa HL, Singh S, Douglas-Jones M, Schermbrucker G, De Lange J, Phoya F, et al. Scurvy masquerading as IgA vasculitis. Pediatr Rheumatol Online J 2024;22:56. doi:10.1186/s12969-024-00992-2.

4) Moser MA, Chun OK. Vitamin C and heart health: A review based on findings from epidemiologic studies. Int J Mol Sci 2016;17:1328. doi: 10.3390/ijms17081328.

5) Golriz F, Donnelly LF, Devaraj S, Krishnamurthy R. Modern American scurvy - experience with vitamin C deficiency at a large children\'s hospital. Pediatr Radiol 2017;47:214-20. doi: 10.1007/s00247-016-3726-4.

6) Polat AV, Bekci T, Say F, Bolukbas E, Selcuk MB. Osteoskeletal manifestations of scurvy: MRI and ultrasound findings. Skeletal Radiol 2015;44:1161-4. doi: 10.1007/s00256-014-2093-1.

7) Milne I, Chalmers I. Documenting the evidence: The case of scurvy. Bull World Health Organ 2004;82:791-6.

8) Amogne W, Nimani M, Shemsedin I, Marshalo W, Jima D, Addissie A, et al. An epidemic of scurvy, identified based on lower extremity swelling, in a Southern Ethiopian Prison. Am J Trop Med Hyg 2021;105:511-6. doi: 10.4269/ajtmh.20- 1246.

9) Bennett M, Coninx R. The mystery of the wooden leg: Vitamin C deficiency in East African prisons. Trop Doct 2005;35:81-4. doi: 10.1258/0049475054036896.