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eMedicine Specialties > Endocrinology > Metabolic Disorders
-----------------------------------------------------------

Vitamin A Toxicity
==================

Author: Mohsen S Eledrisi, MD, FACP, FACE, Consultant, Department of
Internal Medicine, Division of Endocrinology and Metabolism, King
Abdulaziz National Guard Medical Center, Saudi Arabia
Coauthor(s): Kevin McKinney, MD, Assistant Professor, Department of
Medicine, Division of Endocrinology and Metabolism, University of
Texas Medical Branch at Galveston; Mohammad S Shanti, MD, ABEM, Chair,
Department of Emergency Medicine, King Faisal Specialist Hospital and
Research Center
Contributor Information and Disclosures

Updated: Sep 2, 2009

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Overview

Differential Diagnoses & Workup

Treatment & Medication

Follow-up

References

Keywords

Further Reading

Introduction
------------

Background

Vitamin A is an important fat-soluble vitamin. Its basic molecule is a
retinol, or vitamin A alcohol. After absorption, retinol is
transported via chylomicrons to the liver, where it is either stored
as retinol ester or re-exported into the plasma in combination with
retinol-binding protein for delivery to tissue sites.

Dietary vitamin A is obtained from preformed vitamin A (or retinyl
esters), which is found in animal foods (liver, milk, kidney, and fish
oil), fortified foods, and drug supplements. Dietary vitamin A is also
obtained from provitamin A carotenoids from plant sources, principally
carrots. Dietary vitamin A is available mainly as preformed vitamin A
in western countries and as provitamin A carotenoids in developing
countries.

The bioavailability of retinol is generally more than 80%, whereas the
bioavailability and bioconversion of carotenes are lower. These may be
affected by species, molecular linkage, amount of carotene, nutrition
status, genetic factors, and other interactions. While in general the
body absorbs retinoids and vitamin A very efficiently, it lacks the
mechanisms to destroy excessive loads. Thus, the possibility of
toxicity exists unless intake is carefully regulated.1 Revision of
earlier estimates of daily human requirements of vitamin A has been
suggested; the suggestion is that estimates ought to be revised
downwards. Concerns exist about the teratogenicity of vitamin A.2

Pathophysiology

The recommended daily allowance for vitamin A is 5000 international
units (IU) for adults and 8000 IU for pregnant or lactating women.
Being fat-soluble, vitamin A is stored to a variable degree in the
body, making it more likely to cause toxicity when taken in excess
amounts.3 In contrast, water-soluble vitamins are generally excreted
in the urine and stored only to a limited extent; hence, adverse
effects occur only when extremely large amounts are taken.

Frequency

United States

Nutritional surveys indicate that about 35-50% of adults regularly
consume vitamin and mineral supplements. Data are not available for
consumption of vitamins in children.

Mortality/Morbidity

Mortality is rare from vitamin A toxicity.

Morbidity is evident by the wide range of complications observed
 in this condition.

Race

The use of supplements is generally higher in whites, as well
as in individuals with higher levels of education and income.

Sex

The use of vitamin supplements is more common among females.

Age

Single vitamins are consumed more often by adults, while multivitamins
are administered more frequently to children.

Clinical
--------

History

Carotenemia, the ingestion of excessive amounts of vitamin A
 precursors in food, mainly carrots, is manifested by a
 yellow-orange coloring of the skin, primarily the palms of the
 hands and the soles of the feet. It differs from jaundice in that
 the sclerae remain white.

In acute vitamin A toxicity, a history of some or all of the
 following may be obtained:

Nausea

Vomiting

Anorexia

Irritability

Drowsiness

Altered mental status

Abdominal pain

Blurred vision

Headache

Muscle pain with weakness

In chronic vitamin A toxicity, a history of some or all of the
 following may be obtained:

Anorexia

Hair loss

Dryness of mucus membranes

Fissures of the lips

Pruritus

Fever

Headache

Insomnia

Fatigue

Irritability

Weight loss

Bone fracture4

Anemia

Bone and joint pains

Diarrhea

Menstrual abnormalities

Epistaxis

Physical

Manifestations of acute toxicity

Muscle and bone tenderness, especially over the long bones of
 the upper and lower extremities

Neurologic manifestations with signs of increased intracranial
 pressure (eg, children may have bulging fontanelles)

Manifestations of chronic toxicity

Alopecia

Skin erythema

Skin desquamation

Brittle nails

Exanthema

Cheilitis

Conjunctivitis

Petechiae

Liver cirrhosis

Premature epiphysial closure in children

Hepatosplenomegaly

Peripheral neuritis

Benign intracranial hypertension

Ataxia

Papilledema

Diplopia

Hyperostosis

Edema

Hepatic hydrothorax5

Causes

Causes of carotenemia  

Carotenemia is the result of excessive intake of vitamin A
 precursors in foods, mainly carrots.

Other than the cosmetic effect, carotenemia has no adverse
 consequences because the conversion of carotenes to retinol is
 not sufficient to cause toxicity.

Causes of vitamin A toxicity are generally categorized into acute
 and chronic.

Acute toxicity occurs within a few hours or days after a very
 large intake as a result of accidental over-ingestion or
 inappropriate therapy. The estimated toxic dose is about
 25,000 IU/kg.

Chronic toxicity appears after ingestion of 25,000 IU or more
 daily for prolonged periods.

More on Vitamin A Toxicity

Overview: Vitamin A Toxicity

Differential Diagnoses & Workup: Vitamin A Toxicity

Treatment & Medication: Vitamin A Toxicity

Follow-up: Vitamin A Toxicity

References

Further Reading

Next Page »

Print ThisPrint This

Email ThisEmail This

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References
----------

1. 

Maqbool A, Stallings VA. Update on fat-soluble vitamins in cystic
fibrosis. Curr Opin Pulm Med. Nov 2008;14(6):574-81. Medline.

2. 

Mawson AR. On the association between low resting heart rate and
chronic aggression: retinoid toxicity hypothesis. Prog
Neuropsychopharmacol Biol Psychiatry. Mar 17 2009;33(2):205-13. Medline.

3. 

Tan KP, Kosuge K, Yang M, et al. NRF2 as a determinant of cellular
resistance in retinoic acid cytotoxicity. Free Radic Biol Med. Dec
15 2008;45(12):1663-73. Medline.

4. 

Genaro Pde S, Martini LA. Vitamin A supplementation and risk of
skeletal fracture. Nutr Rev. Feb 2004;62(2):65-7. Medline.

5. 

Miksad R, Ledinghen V, McDougall C, et al. Hepatic hydrothorax
associated with vitamin A toxicity. J Clin Gastroenterol. 2002;34:275-279. Medline.

6. 

Bhalla K, Ennis DM, Ennis ED. Hypercalcemia caused by iatrogenic
hypervitaminosis A. J Am Diet Assoc. 2005;105:119-121. Medline.

7. 

Johnson-Davis KL, Moore SJ, Owen WE, et al. A rapid HPLC method
used to establish pediatric reference intervals for vitamins A and
E. Clin Chim Acta. Jul 2009;405(1-2):35-8. Medline.

8. 

Barker ME, Blumsohn A. Is vitamin A consumption a risk factor for
osteoporotic fracture?. Proc Nutr Soc. 2003;62:845-850. Medline.

9. 

Bates CJ. Vitamin A. Lancet. Jan 7 1995;345(8941):31-5. Medline.

10. 

Hathcock JN. Vitamins and minerals: efficacy and safety. Am J Clin
Nutr. Aug 1997;66(2):427-37. Medline.

11. 

Hathcock JN, Hattan DG, Jenkins MY, et al. Evaluation of vitamin A
toxicity. Am J Clin Nutr. Aug 1990;52(2):183-202. Medline.

12. 

Michaelsson K, Lithell H, Vessby B, et al. Serum retinol levels
and the risk of fracture. N Engl J Med. 2003;348:287-294. Medline.

13. 

Nagai K, Hosaka H, Kubo S, et al. Vitamin A toxicity secondary to
excessive intake of yellow-green vegetables, liver and laver. J
Hepatol. Jul 1999;31(1):142-8. Medline.

14. 

O'Donnell J. Polar hysteria: an expression of hypervitaminosis A. Am
J Ther. 2004;11:507-516. Medline.

15. 

Olson JA. Adverse effects of large doses of vitamin A and
retinoids. Semin Oncol. Sep 1983;10(3):290-3. Medline.

16. 

Penniston KL, Tanumihardjo S. The acute and chronic toxic effects
of vitamin A. Am J Clin Nutr. 2006;83:191-201.

17. 

Perrotta S, Nobili B, Rossi F, et al. Infant hypervitaminosis A
causes severe anemia and thrombocytopenia: evidence of a
retinol-dependent bone marrow cell growth inhibition. Blood. 2002;99:2017-2022. Medline.

18. 

Sharieff GQ, Hanten K. Pseudotumor cerebri and hypercalcemia
resulting from vitamin A toxicity. Ann Emerg Med. Apr 1996;27(4):518-21. Medline.

CLOSE WINDOW 

Further Reading
---------------

Related eMedicine topics:
Avitaminosis A
Carotenemia Dermatology
Carotenemia Pediatrics: General Medicine
Toxicity, Vitamin
Vitamin A Deficiency
Vitamin E Toxicity

CLOSE WINDOW 

Keywords
--------

vitamin A toxicity, vitamin A, retinol, carotene, vitamin
carotene, retinoid, carotenemia, isotretinoin, Accutane, carotenes,
vitamin A alcohol, retinol ester, vitamin A overdose, vitamin A
poisoning, dietary vitamin A, vitamin A supplements, provitamin A
carotenoids

CLOSE WINDOW 

Contributor Information and Disclosures
---------------------------------------

Author

Mohsen S Eledrisi, MD, FACP, FACE, Consultant, Department of Internal
Medicine, Division of Endocrinology and Metabolism, King Abdulaziz
National Guard Medical Center, Saudi Arabia
Mohsen S Eledrisi, MD, FACP, FACE is a member of the following medical
societies: American Association of Clinical Endocrinologists, American
College of Physicians-American Society of Internal Medicine, American
Diabetes Association, American Medical Association, and Endocrine
Society
Disclosure: Nothing to disclose.

Coauthor(s)

Kevin McKinney, MD, Assistant Professor, Department of Medicine,
Division of Endocrinology and Metabolism, University of Texas Medical
Branch at Galveston
Kevin McKinney, MD is a member of the following medical societies:
Texas Medical Association
Disclosure: Nothing to disclose.

Mohammad S Shanti, MD, ABEM, Chair, Department of Emergency Medicine,
King Faisal Specialist Hospital and Research Center
Mohammad S Shanti, MD, ABEM is a member of the following medical
societies: American Academy of Emergency Medicine, American College of
Emergency Physicians, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Medical Editor

Harris C Taylor, MD, Clinical Professor of Medicine, Division of
Clinical and Molecular Endocrinology, Case Western Reserve University
School of Medicine
Harris C Taylor, MD is a member of the following medical societies:
American Association of Clinical Endocrinologists, American College of
Physicians, American Thyroid Association, and Endocrine Society
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Romesh Khardori, MD, Chief, Division of Endocrinology, Metabolism and
Molecular Medicine, Professor, Department of Internal Medicine,
Southern Illinois University School of Medicine
Romesh Khardori, MD is a member of the following medical societies:
American Association of Clinical Endocrinologists, American College of
Physicians, American Diabetes Association, American Federation for
Medical Research, American Medical Association, American Society of
Andrology, Endocrine Society, and Illinois State Medical Society
Disclosure: Nothing to disclose.

CME Editor

Mark Cooper, MBBS, PhD, FRACP, Head, Diabetes & Metabolism Division,
Baker Heart Research Institute, Professor of Medicine, Monash
University
Disclosure: Nothing to disclose.

Chief Editor

George T Griffing, MD, Professor of Medicine, St Louis University
School of Medicine
George T Griffing, MD is a member of the following medical societies:
American Association for the Advancement of Science, American College
of Medical Practice Executives, American College of Physician
Executives, American College of Physicians, American Diabetes
Association, American Federation for Medical Research, American Heart
Association, Central Society for Clinical Research, Endocrine Society,
International Society for Clinical Densitometry, and Southern Society
for Clinical Investigation
Disclosure: Nothing to disclose.

Search for CME/CE on This Topic »

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