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Dermatologic Manifestations of Vitamin A Deficiency Clinical Presentation

  • Author: Robert A Schwartz, MD, MPH; Chief Editor: William D James, MD  more...
Updated: Jun 09, 2016


Avitaminosis A generally accompanies states of severe malnutrition, such as kwashiorkor and marasmus, and may be suspected in individuals with an unusual susceptibility to infectious diseases, such as measles. Note the following:

  • Impaired vision, particularly at night: Because of the essential role of vitamin A in photoreceptor function, night blindness is the earliest and most common symptom of its deficiency.
  • Xerophthalmia: VAD may produce xerophthalmia. Its ocular manifestations include conjunctival and corneal xerosis (drying), keratomalacia (corneal necrosis/ulceration), nyctalopia (night blindness), and Bitot spots (conjunctival lesions). [4] Maternal night blindness is common during pregnancy in poor countries. Maternal night blindness during pregnancy has been associated with low birthweight, morbidity, and poor growth in South India. [13]
  • Photophobia
  • Erythema
  • Dry, thickened skin (toad skin)
  • Diarrhea
  • Recent history of biliopancreatic diversion bariatric surgery, with phrynoderma and ocular symptoms rarely noted [14, 15]


The most distinctive clinical features of VAD are present in the ocular system; however, numerous skin findings have also been reported.

Conjunctival xerosis is typically found on the temporal, interpalpebral, and bulbar conjunctivae. Characteristically, it is seen as a dry, granular patch that can exhibit thickening, wrinkling, loss of pigmentation, and transparency.

Bitot spots are triangular, perilimbal, gray plaques of keratinized conjunctival debris overlying an area of conjunctival xerosis.

Xerophthalmia results from instability of the precorneal tear film, which can lead to a dull corneal appearance and a superficial punctate keratopathy noted with the use of fluorescein.

Corneal ulcerations can be partial or full thickness. Keratomalacia is a full-thickness liquefactive necrosis of the cornea. Clinically, it is a sharply demarcated lesion with an opaque, grayish yellow appearance. The stroma can slough, either leaving a descemetocele or, in severe cases, causing perforation and loss of the anterior chamber.

Generalized xerosis with fine wrinkles and scales may be present.

Phrynoderma (follicular hyperkeratosis) is characterized by red-brown follicular papules that are approximately 2-6 mm in diameter, with a central keratotic spinous plug. These lesions are usually found clustered around the bony prominences of the elbows and the knees, although they may extend up the thighs and the arms.



VAD occurs where diets contain insufficient amounts of vitamin A for growth and development, physiological functions, and periods of added stress due to illness.[16]

Avitaminosis A is often diagnosed in persons with alcoholism who are malnourished and in patients who are chronically ill with intestinal malabsorption disorders, such as sprue, bypass surgery, cystic fibrosis, pancreatitis, metastatic cancer, regional enteritis, and chronic gastroenteritis. Other patients with avitaminosis A include those with liver disease that causes abnormal or decreased storage of vitamin A. Patients receiving total parenteral nutrition can also show signs and symptoms of avitaminosis A secondary to loss of vitamin A with prolonged use.

Avitaminosis A is a problem wherever the combination of vitamin A and protein deficiency exists. In developed countries, VAD is a rare condition. However, it is a problem of enormous magnitude worldwide, particularly in the underdeveloped regions of Asia, where the diet often consists of little more than rice. Avitaminosis A is fairly well controlled in much of Latin America and the Caribbean, with the exception of Haiti, where the incidence is as high as that in some Asian countries. Some reports suggest that the prevalence of xerophthalmia in parts of Africa may be as high as that found in Southeast Asia, whereas in other areas, particularly West Africa, the prevalence is lower, mostly because the red palm oil widely used for cooking is a good source of vitamin A supplementation. In endemic countries, the disease is largely confined to lower socioeconomic groups who cannot afford vitamin A–rich foods.

Women of childbearing age are at high risk of VAD and its consequences because of increased vitamin A requirements during pregnancy and lactation. Their newborns, having been vitamin A depleted, require vitamin A supplements. Otherwise, after the initial 4-6 months of breastfeeding, the babies are likely to develop VAD.

Infections, such as measles, may precipitate a child into clinical VAD.[17, 18]

VAD can be assumed to have profound effects because vitamin A supplementation reduces child mortality and severe morbidity in underdeveloped countries. Vitamin A supplementation enhances infants' immune responses to hepatitis B vaccine.[19]

Contributor Information and Disclosures

Robert A Schwartz, MD, MPH Professor and Head of Dermatology, Professor of Pathology, Pediatrics, Medicine, and Preventive Medicine and Community Health, Rutgers New Jersey Medical School; Visiting Professor, Rutgers University School of Public Affairs and Administration

Robert A Schwartz, MD, MPH is a member of the following medical societies: Alpha Omega Alpha, New York Academy of Medicine, American Academy of Dermatology, American College of Physicians, Sigma Xi

Disclosure: Nothing to disclose.


Santiago A Centurion, MD Dermatologist, Dermatology Associates of Central NJ

Santiago A Centurion, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Society for Dermatologic Surgery, American Society for MOHS Surgery, American Society of Dermatopathology, Sigma Xi

Disclosure: Nothing to disclose.

Pere Gascon, MD, PhD Professor and Director, Division of Medical Oncology, Institute of Hematology and Medical Oncology, IDIBAPS, University of Barcelona Faculty of Medicine, Spain

Pere Gascon, MD, PhD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, New York Academy of Medicine, New York Academy of Sciences, Sigma Xi

Disclosure: Nothing to disclose.

Specialty Editor Board

David F Butler, MD Section Chief of Dermatology, Central Texas Veterans Healthcare System; Professor of Dermatology, Texas A&M University College of Medicine; Founding Chair, Department of Dermatology, Scott and White Clinic

David F Butler, MD is a member of the following medical societies: American Medical Association, Alpha Omega Alpha, Association of Military Dermatologists, American Academy of Dermatology, American Society for Dermatologic Surgery, American Society for MOHS Surgery, Phi Beta Kappa

Disclosure: Nothing to disclose.

Jeffrey J Miller, MD Associate Professor of Dermatology, Pennsylvania State University College of Medicine; Staff Dermatologist, Pennsylvania State Milton S Hershey Medical Center

Jeffrey J Miller, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, Society for Investigative Dermatology, Association of Professors of Dermatology, North American Hair Research Society

Disclosure: Nothing to disclose.

Chief Editor

William D James, MD Paul R Gross Professor of Dermatology, Vice-Chairman, Residency Program Director, Department of Dermatology, University of Pennsylvania School of Medicine

William D James, MD is a member of the following medical societies: American Academy of Dermatology, Society for Investigative Dermatology

Disclosure: Nothing to disclose.

Additional Contributors

Shyam Verma, MBBS, DVD, FAAD Clinical Associate Professor, Department of Dermatology, University of Virginia School of Medicine; Adjunct Associate Professor, Department of Dermatology, State University of New York at Stonybrook School of Medicine; Adjunct Associate Professor, Department of Dermatology, University of Pennsylvania School of Medicine

Shyam Verma, MBBS, DVD, FAAD is a member of the following medical societies: American Academy of Dermatology

Disclosure: Nothing to disclose.


The authors and editors of Medscape Reference gratefully acknowledge the contributions of previous author, Cristina S. Solis, MD, to the development and writing of this article.

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