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Scurvy in 2017 in the USA.

Scurvy, a disease caused by a deficiency of vitamin C, is uncommon in the modern era and is often under-diagnosed. Vitamin C serves as a cofactor in collagen synthesis, and its deficiency is characterized by hemorrhagic diathesis. We describe a case of scurvy presenting with anemia, perifollicular hemorrhages, and extensive ecchymoses and highlight the importance of recognizing vitamin C deficiency as a cause of bleeding diathesis.


A 65-year-old man with known anxiety-depression and emphysema (smoker for 30 years) presented with dyspnea and dizziness. He lived alone and his diet consisted of carbohydrates and lacked fresh fruits and vegetables. Current medications included only duloxetine and bronchodilators. Physical examination disclosed perifollicular hemorrhages and extensive ecchymoses with increased pigmentation involving the lower extremities (Figure 1). Duloxetine was discontinued; nevertheless, he developed a right thigh hematoma. Laboratory evaluation is summarized in Table 1. Vitamin C levels were <5 [micro]mol/L (normal 23-114 [micro]mol/L). Vitamin C supplements were administered with dramatic dissipation of ecchymosis and improvement of anemia (Figure 2).


Scurvy, known since the Egyptian era, is rarely seen in the modern world due to the discovery of its link to the dietary deficiency of vitamin C. Scurvy was first described in sea voyagers by the Elbers papyrus in 1550 BC. Humans cannot synthesize vitamin C and hence require an exogenous source. (1) Following ingestion, ascorbic acid (AA) is absorbed in the small intestine, and excess amounts are excreted in urine. Although vitamin C is readily stored in tissues throughout the body, these stores are quickly exhausted. Serum AA is three times lower in smokers than in nonsmokers, significantly increasing their chances of AA deficiency. (2) Smokers possess a 40% increase in daily vitamin C turnover, increasing the potential for vitamin C deficiency in smokers who consume < 200 mg/d of vitamin C. Other risk factors include living alone (particularly for men), advanced age, long-term alcoholism, and a voluntarily restrictive diet lacking vegetables and fruits. (3)

The critical role of vitamin C in humans is collagen synthesis. Collagen is an essential element in skin and blood vessels. (4) Vitamin C helps to hydroxylate excess proline and lysine in procollagen, stabilizing the triple helix. Malfunction in collagen synthesis is the primary cause of clinical manifestations of vitamin C deficiency. (5) Thus, it eventually leads to skin lesions and ruptured blood vessels. Vitamin C levels in the body become undetectable 41 days following dietary lack of vitamin C. Cell depletion commences after 121 days, and dermal lesions appear at 132 days following dietary vitamin C deprivation.

Early manifestations include nonspecific fatigue, lassitude, and depression and hence diagnosis is often delayed, as occurred in our patient, until cutaneous manifestations occur. Dermatological manifestations are the hallmark of scurvy and range from paleness, bloated complexion, dryness, and follicular hyperkeratosis to hemorrhagic skin lesions and spontaneous hematomas. (6) Oral findings include gingivitis, periodontitis, and mucosal hemorrhages. Ocular manifestations like conjunctival hemorrhage and flame-shaped hemorrhages of the fundus may also be evident. Late presentations include bone pain, leg edema, dyspnea, anxiety, anorexia, pulmonary hypertension, leukopenia, syncope, hypotension, and eventually death unless the vitamin C deficiency is corrected in a timely manner. Diagnosis is usually made by the impressive clinical findings discussed above and the dramatic response to vitamin C therapy; nevertheless, measurement of ascorbic acid levels aids the clinical diagnosis. Repleting the body stores and correcting the critical deficiency of AA remain the goals of therapy. AA at a dose of 300 mg for 1 month cures most of the symptoms and signs within 4 weeks, with complete recovery expected in 3 months.7


Krishna M. Baradhi

(1.) Fraser IM, Dean M. Extensive bruising secondary to vitamin C deficiency. BMJ Case Rep. 2009; 2009:bcr20080750.

(2.) Schectman G. Estimating ascorbic acid requirements for cigarette smokers. Ann N YAcad Sci. 1993; 686:335-345; discussion 345-346.

(3.) Fain O. Musculoskeletal manifestations of scurvy. Joint Bone Spine. 2004; 72:124-128.

(4.) Kocak M, Akbay G, Eksioglu M. Case 2. Clin Exp Dermatol. 2003; 28:337-338.

(5.) Mapp SJ, Caughlin PB. Scurvy in an otherwise well young man. Med J Aust. 2006; 185:331-332.

(6.) Stewart CP, Guthrie D. Lind's Treatise on Scurvy, a Bicentennial Volume Containing a Reprint of the First Edition of A Treatise on Scurvy by James Lind, MD, with Additional Notes. Edinburgh, Scotland: Edinburgh University Press; 1953.

(7.) Hodges RE. Scurvy. Nutrition in preventive medicine. Monogr Ser World Health Organ. 1976; 62:20-25.

Krishna M. Baradhi, MD (a), Shobana Vallabhaneni, MBBS (b), and Supriya Koya, MD (c)

(a) Division of Nephrology, University of Oklahoma, Tulsa, Oklahoma; (b) Department of Medicine, University of Chongqing Medical University, Chongqing, P. R. China; department of Hematology and Oncology, Utica Park Clinic Oncology, Tulsa, Oklahoma

Corresponding author: Krishna M. Baradhi, MD, Division of Nephrology, University of Oklahoma, Tulsa, 4502 E. 41st Street, OU-Tulsa Schusterman Center, Tulsa, OK 74135 (e-mail:

Received October 29, 2017; Revised December 17, 2017; Accepted December 21, 2017.

Caption: Figure 1. Right arrow showing perifollicular hemorrhages and left arrow showing extensive ecchymosis.

Caption: Figure 2. (a) Extensive ecchymosis of the lower extremity prior to the treatment. (b) Resolution of ecchymosis after vitamin C treatment.
Table 1. Laboratory findings

Lab test                               Patient's value   Normal values

Hemoglobin (g/dL)                            8.3          13.5-17.5
Platelet count ([10.sup.9]/L)              165,000       150-450,000
Reticulocyte count                          4.5%          0.4%-2.4%
Prothrombin time (seconds)                   13             11-14
Partial thromboplastin time (seconds)        30             20-39
Alpha 2-antiplasmin levels                  153%          85%-156%
Euglobulin lysis time (minutes)              >60           90-240
Platelet function analysis
  Collagen ADP (seconds)                     81            55-137
  Collagen epinephrine (seconds)             123           78-199
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Author:Baradhi, Krishna M.; Vallabhaneni, Shobana; Koya, Supriya
Publication:Baylor University Medical Center Proceedings
Article Type:Clinical report
Geographic Code:1USA
Date:Apr 1, 2018
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