eMedicine Specialties > Dermatology > Metabolic Diseases

Scurvy: Treatment & Medication

Author: Anne Laumann, MB, ChB, MRCP(UK), FAAD, Associate Professor, Department of Dermatology, Feinberg School of Medicine, Northwestern University
Coauthor(s): Julia Sanger Minocha, MD, Resident Physician, Department of Medicine, Feinberg School of Medicine, Northwestern University; Janet J Wong, MD, Consulting Dermatologist, Department of Dermatology, University of Connecticut
Contributor Information and Disclosures

Updated: Jan 21, 2009

Treatment

Medical Care

  • Scurvy is treated with ascorbic acid.
  • Patients who undergo dialysis should receive 500 mg of supplemental vitamin C daily.
  • Patients benefit from a daily multivitamin because of potential coexisting nutritional deficiencies.

Consultations

  • Consult a dermatologist for evaluation of skin findings.
  • Consult a nutritionist for evaluation of diet, nutritional education, and assistance.
  • Consult an internal medicine specialist for evaluation of systemic findings.

Diet

  • As little as 6-10 mg of vitamin C a day is sufficient to maintain body stores of more than 350 mg. Higher intakes are recommended for smokers and pregnant women. Fresh fruits and vegetables are the best sources of vitamin C. A small orange contains approximately 50 mg of vitamin C. In the United States, many beverages are fortified with vitamin C.

Medication

The goal of treatment of scurvy is to saturate the body rapidly with ascorbic acid. At maximum doses, body stores become saturated in a few days. With proper treatment, bleeding stops within 24 hours, and perifollicular petechiae resolve in 2 weeks.

Vitamins

Vitamins are essential for normal DNA synthesis and cell function.


Ascorbic acid (Vitamin C)

For collagen synthesis and tissue repair.

Adult

2 g PO/IV/PO qd for first 2 d, then 500 mg PO/IV qd for 1 wk; alternatively, 100 mg tid for 1 wk, then 100 mg qd for several wk until tissue saturation is normal

Pediatric

Prophylactic dose for infants on formula feedings: 35 mg/d PO/IM for first few wk of life; if formula contains 2-3 times amount of protein in human milk, dose should be 50 mg/d PO/IM (AMA Council on Drugs, 1980)

Decreases effects of warfarin and fluphenazine; increases aspirin levels; on occasion has been used as a specific antidote for symptoms resulting from interaction between ethanol and disulfiram; ascorbic acid in the urine may interfere with tests for glycosuria; concomitant administration of amygdalin and high doses of ascorbic acid may lead to cyanide toxicity by increasing conversion of amygdalin to hydrogen cyanide and by vitamin C – dependent depletion of body stores of cysteine, which is used to detoxify cyanide; doses as low as 250 mg may destroy up to 81% of cyanocobalamin in a moderate vitamin B-12 – containing meal and up to 25% in high vitamin B-12 – containing meal; coadministration of indinavir with high-dose ascorbic acid (vitamin C) may significantly reduce serum concentrations of indinavir

Documented hypersensitivity; large doses (given in pregnancy reported to cause scurvy in neonates removed from vitamin C–rich fetal environment)

Pregnancy

A - Fetal risk not revealed in controlled studies in humans

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

High doses should not be taken by diabetic patients, people on anticoagulant therapy, or those with a history of renal calculi or gout; RDA for lactating mothers is 90-100 mg (excreted in breast milk); caution in concurrent sodium-restricted diet; patients undergoing stool occult blood tests; some brands of injectable vitamin C contain sulfites, which can cause allergic reactions, including anaphylaxis, in susceptible individuals; some brands contain benzyl alcohol (avoid in premature infants); because of pressure build-up in ampules, wrap ampule with covering while opening

More on Scurvy

Overview: Scurvy
Differential Diagnoses & Workup: Scurvy
Treatment & Medication: Scurvy
Follow-up: Scurvy
References
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References

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  2. Noble JM, Mandel A, Patterson MC. Scurvy and rickets masked by chronic neurologic illness: revisiting "psychologic malnutrition". Pediatrics. Mar 2007;119(3):e783-90. [Medline].

  3. Duggan CP, Westra SJ, Rosenberg AE. Case records of the Massachusetts General Hospital. Case 23-2007. A 9-year-old boy with bone pain, rash, and gingival hypertrophy. N Engl J Med. Jul 26 2007;357(4):392-400. [Medline].

  4. Arron ST, Liao W, Maurer T. Scurvy: a presenting sign of psychosis. J Am Acad Dermatol. Aug 2007;57(2 Suppl):S8-10. [Medline].

  5. Delanghe JR, Langlois MR, De Buyzere ML, Torck MA. Vitamin C deficiency and scurvy are not only a dietary problem but are codetermined by the haptoglobin polymorphism. Clin Chem. Aug 2007;53(8):1397-400. [Medline].

  6. Emadi-Konjin P, Verjee Z, Levin AV, Adeli K. Measurement of intracellular vitamin C levels in human lymphocytes by reverse phase high performance liquid chromatography (HPLC). Clin Biochem. May 2005;38(5):450-6. [Medline].

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Further Reading

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Keywords

infantile scurvy, Barlow disease, Barlow's disease, vitamin C deficiency, ascorbic acid, widower scurvy, chronic malnutrition

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Contributor Information and Disclosures

Author

Anne Laumann, MB, ChB, MRCP(UK), FAAD, Associate Professor, Department of Dermatology, Feinberg School of Medicine, Northwestern University
Anne Laumann, MB, ChB, MRCP(UK), FAAD is a member of the following medical societies: American Academy of Dermatology, Association of Professors of Dermatology, Chicago Dermatological Society, Chicago Medical Society, Illinois Dermatological Society, Illinois State Medical Society, Illinois State Medical Society, Medical Dermatology Society, and Society for Investigative Dermatology
Disclosure: Nothing to disclose.

Coauthor(s)

Julia Sanger Minocha, MD, Resident Physician, Department of Medicine, Feinberg School of Medicine, Northwestern University
Julia Sanger Minocha, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, and Phi Beta Kappa
Disclosure: Nothing to disclose.

Janet J Wong, MD, Consulting Dermatologist, Department of Dermatology, University of Connecticut
Janet J Wong, MD is a member of the following medical societies: American Academy of Dermatology
Disclosure: Nothing to disclose.

Medical Editor

Kathryn Schwarzenberger, MD, Associate Professor of Medicine, Division of Dermatology, University of Vermont College of Medicine; Consulting Staff, Division of Dermatology, Fletcher Allen Health Care
Kathryn Schwarzenberger, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Contact Dermatitis Society, American Dermatological Association, Dermatology Foundation, Medical Dermatology Society, and Women's Dermatologic Society
Disclosure: Nothing to disclose.

Pharmacy Editor

Michael J Wells, MD, Associate Professor, Department of Dermatology, Texas Tech University Health Sciences Center
Michael J Wells, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, and Texas Medical Association
Disclosure: Nothing to disclose.

Managing Editor

Van Perry, MD, Assistant Professor, Department of Medicine, Division of Dermatology, University of Texas Health Science Center
Van Perry, MD is a member of the following medical societies: American Academy of Dermatology and American Society for Laser Medicine and Surgery
Disclosure: Nothing to disclose.

CME Editor

Catherine Quirk, MD, Clinical Assistant Professor, Department of Dermatology, Brown University
Catherine Quirk, MD is a member of the following medical societies: Alpha Omega Alpha and American Academy of Dermatology
Disclosure: Nothing to disclose.

Chief Editor

Dirk M Elston, MD, Director, Department of Dermatology, Geisinger Medical Center
Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology
Disclosure: Nothing to disclose.

 
 
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