U.S. flag

An official website of the United States government

NCBI Bookshelf. A service of the National Library of Medicine, National Institutes of Health.

StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan-.

Cover of StatPearls

StatPearls [Internet].

Show details

Vitamin A Toxicity

; ; .

Author Information and Affiliations

Last Update: September 2, 2023.

Continuing Education Activity

Vitamin A plays a crucial role in regulating various physiological processes of the body and maintaining vision and immune system function to support skin health and cell growth. Although vitamin A is essential for the body, excessive intake can pose various adverse effects, disrupting the body's equilibrium and overall well-being. Vitamin A toxicity, also known as hypervitaminosis A, can result from either the excessive consumption of vitamin A and related compounds or its topical application. This activity describes the causes, evaluation, management, treatment, and prevention of vitamin A toxicity, emphasizing the essential role of the interprofessional healthcare team in enhancing care for affected patients.


  • Identify the risk factors associated with excessive vitamin A intake, considering dietary sources, supplements, and medication history.
  • Assess laboratory findings, including serum vitamin A levels, liver function tests, lipid profiles, and hematological parameters, to diagnose and monitor vitamin A toxicity in patients.
  • Select and recommend appropriate treatment modalities, alternative therapies, or supplements to patients based on the severity and presentation of vitamin A toxicity.
  • Coordinate with the interprofessional healthcare team to guide pregnant women about safe vitamin A use during pregnancy and prevent teratogenic malformations.
Access free multiple choice questions on this topic.


Vitamin A is essential for maintaining the body's vision, cell division, reproduction, and immune function. Vitamin A belongs to the category of lipid-soluble compounds called retinoic acids. Beta-carotene is the most well-known form of 2 clinically significant forms of vitamin A: preformed vitamin A and provitamin A carotenoids. Mammals metabolize carotenoids into active vitamin A. Preformed vitamin A encompasses metabolically active compounds such as retinol, retinal, retinoic acid, and retinyl esters. Although essential for overall health, excessive consumption of preformed vitamin A can lead to acute and chronic toxicity. The condition characterized by elevated levels of vitamin A in the body is referred to as hypervitaminosis A. Vitamin A, also known as teratogen, is capable of causing severe malformations. This article comprehensively reviews the prevention, presentation, laboratory findings, and treatment of the 3 recognized syndromes of vitamin A toxicity: acute, chronic, and teratogenic.


Hypervitaminosis A is relatively uncommon and usually arises from excessive supplementation or medication usage. The primary cause of toxicity is the consumption of substantial quantities of vitamin A through dietary supplements and foods. This usually occurs when individuals consume high doses of vitamin A without proper medical supervision. Most diets contain a combination of preformed vitamin A and provitamin A carotenoids. Preformed vitamin A is derived from animal sources and is found in egg yolks, butter, chicken, beef, organ meats, fish, fish oils, and fortified foods.[1] Preformed vitamin A is readily absorbed in the small intestine and subsequently stored in the liver. Therefore, excessive intake of dietary preformed vitamin A from animal-based sources and supplements can contribute to the risk of toxicity. 

Provitamin A carotenoids, such as beta-carotene, are plant pigments that the body converts into active vitamin A. These carotenoids are plentiful in leafy greens and vibrantly colored vegetables and fruits, including carrots, sweet potatoes, and papayas.[2] The absorption of provitamin A is variable and subject to feedback regulation, making it unlikely to lead to toxicity with excessive intake.[3] Certain dermatological medications, such as isotretinoin, contain analogs of vitamin A. Prolonged or excessive usage of these medications can lead to an accumulation of vitamin A stores, resulting in hypervitaminosis A, toxicity, and teratogenic effects.

The recommended daily allowance (RDA) for vitamin A is measured in retinol activity equivalents (RAE) to account for the different bioactivities of retinol and provitamin A carotenoids. Notably, 1 RAE is equivalent to 1 mcg of retinol or 3 International units (IU).

The RDA for vitamin A is as follows:

  • 700 RAE for adult women
  • 900 RAE for adult men
  • 750 to 770 RAE for pregnant women
  • 1200 to 1300 RAE for lactating women

The tolerable upper intake levels (UL) for vitamin A have been established to prevent toxicity. The UL of vitamin A for adults is 3000 RAE per day, including preformed vitamin A from foods and supplements and the amount that can be converted from plant-based sources such as beta-carotene. The consumption of preformed vitamin A from dietary supplements in developed countries frequently surpasses the RDA.[4]


Few published reports of vitamin A toxicity have been published, with fewer than 10 cases per year documented from 1976 to 1987.[5] Infants and children are at a higher risk of toxicity due to their smaller body size and reduced tolerance for high doses.[6] Accidental ingestion of vitamin A supplements by children is a common cause of acute toxicity. There is no substantial difference in the occurrence of vitamin A toxicity between males and females. However, pregnant women are at risk if they take high doses of vitamin supplements.

Excessive supplement intake typically occurs in developed countries when individuals exceed the RDA.[4] Supplementation programs have been implemented in regions where vitamin deficiency is a significant public health concern. Moreover, toxicity can arise if dosing guidelines are not carefully followed.[7][8] Populations heavily reliant on liver-based food sources rich in vitamin A, such as polar bear liver and chicken liver, face an increased risk of vitamin A toxicity. However, only rare cases of this phenomenon are reported in the published literature, and it is not considered a significant public health concern.[9][10][11]


The symptoms of systemic vitamin A toxicity vary depending on the severity and duration of excessive intake. The 3 recognized syndromes of vitamin A toxicity are acute, chronic, and teratogenic.

Acute systemic vitamin A toxicity typically arises when an individual consumes over 100,000 RAE within a short period, often from supplements or high-dose medications. The toxicity symptoms include nausea, vomiting, headache, dizziness, irritability, blurred vision, and muscular incoordination. Acute toxicity is rare and is more likely to occur after consuming synthetic forms of vitamin A, such as the retinoid medication isotretinoin. Mucocutaneous effects include cheilitis and dryness of lips and oral, ophthalmic, and nasal mucosa. The suggested mechanism involves decreased sebum production, reduced epidermal thickness, and altered barrier function. Additional cutaneous effects include dry skin, pruritus, peeling of the palms and soles, and fissuring of the fingertips. Higher doses of vitamin A may lead to telogen effluvium. Severe cases may manifest with bone pain and increased intracranial pressure.

Chronic vitamin A toxicity is associated with prolonged ingestion of excessive vitamin A, typically exceeding 8000 RAE per day. This condition can develop after consuming substantial quantities of animal-based foods rich in preformed vitamin A, such as liver, or through the prolonged use of high-dose vitamin A supplements.[12] The toxicity symptoms include dry, cracked skin, hair loss, brittle nails, fatigue, loss of appetite, bone and joint pain, and hepatomegaly. Chronic retinoid toxicity affects various organ systems. Bone-related effects include bone spurs, calcinosis, and bone resorption, leading to hypercalcemia, osteoporosis, and hip fractures.[13][14] Central nervous system effects include headache, nausea, and vomiting.

Pseudotumor cerebri syndrome has been associated with vitamin A toxicity.[15] Hypothyroidism, reversible upon discontinuation of therapy, was observed in 40% of patients during clinical trials for cutaneous T-cell lymphoma with bexarotene, a derivative of vitamin A.[16] Reversible renal dysfunction with elevated serum creatinine has been observed after etretinate use, but not after isotretinoin use.[17] Etretinate, a psoriasis medication, is no longer prescribed in most countries because of its teratogenic effects.

Hypertriglyceridemia is the most common laboratory abnormality associated with oral retinoid use. Triglyceride, low-density lipoprotein, and total cholesterol levels increase in many patients using bexarotene, isotretinoin, etretinate, and acitretin.[18][19] Elevated serum transaminases may also occur with oral retinoid usage, more often with etretinate or acitretin compared to isotretinoin and bexarotene. These levels typically show an increase within 2 to 8 weeks after the initiation of therapy, followed by normalization over the subsequent 2 to 4 weeks. Prolonged liver damage can include fibrosis and cirrhosis.[20] No definitive causal association has been established between isotretinoin and depression, psychosis, or suicide attempts, although such a link had been previously suggested.[21]

The teratogenic effects of vitamin A intake were first discovered in animal studies during the 1950s. Subsequently, extensive research has been conducted to elucidate the underlying causes of the effects.[22] Excessive vitamin A consumption during pregnancy has been associated with various congenital malformations in humans. The disabilities associated with this condition include abnormalities in the central nervous system, such as microcephaly and hydrocephalus; cardiac issues, such as transposition of the great vessels; craniofacial deformities, such as cleft lip and palate; limb abnormalities; and urinary tract disorders.[5][3] 

Vitamin A is critical for regulating gene expression and guiding cell differentiation during embryonic development. The embryo is particularly susceptible to the teratogenic effects of excessive amounts of vitamin A during the first trimester, which is a phase marked by rapid organogenesis. Teratogenic effects are primarily associated with high doses of retinoid medications such as isotretinoin rather than dietary sources of vitamin A. A minimum safe dose of oral retinoids during pregnancy has not been established. Isotretinoin is estimated to increase the risk of fetal malformations by 25-fold.[5] The mechanism is believed to be linked to a toxic effect on neural crest cells, possibly affecting the regulation of axial patterning in the embryo via the expression of the homeobox gene Hoxb-1.[23] 

Pregnant women should refrain from using oral retinoid medications and excessive vitamin A supplements to mitigate the risk of vitamin A-related malformations. They should consult healthcare professionals and prenatal care providers to ensure proper prenatal nutrition and avoid drugs or supplements that are contraindicated during pregnancy. Prescribers should only recommend oral retinoids to women of childbearing age who are not pregnant and use reliable birth control methods to prevent the potential risk of vitamin A-related teratogenic effects. 


Hypervitaminosis A affects multiple organ systems of the body and can damage the liver, bones, central nervous system, and skin. The specific histopathological findings differ based on the severity and duration of the toxicity, some of which are listed below.

Liver: Hepatic steatosis, hepatocellular injury, and fibrosis with collagen deposits

Bone: Osteoporosis and thickening of cortical bone

Central nervous system: Pseudotumor cerebri and cerebral edema

Skin: Exfoliative dermatitis and epidermal hyperplasia [24][25]


The toxicokinetics of vitamin A toxicity involve its absorption, distribution, metabolism, and elimination from the body.

Absorption: Dietary vitamin A is sourced from 2 main categories: preformed vitamin A, including retinol and retinyl esters, which are found in animal-derived products and supplemented foods, and provitamin A carotenoids present in fruits and vegetables. High-fat meals enhance the absorption of vitamin A in the small intestine.

Distribution: After absorption, vitamin A is transported to the liver, where it is stored as retinyl esters. From there, it is released into the bloodstream bound to retinol-binding protein (RBP) and transthyretin. These carrier proteins help transport vitamin A to target tissues, including the eyes, skin, and other organs.

Metabolism: Retinol is converted into its active forms, retinal and retinoic acid, within target tissues. Lecithin retinol acyltransferase (LRAT) is the enzyme responsible for catalyzing retinoid esterification for storage in the liver.[26] Cellular RBP assists LRAT in regulating retinoid uptake and metabolism. These 2 proteins are essential in the metabolism of retinoids, which may be responsible for the toxic effects of vitamin A.

Elimination: Fat-soluble vitamin A and its metabolites are primarily excreted through bile and feces, with only a small portion being eliminated in the urine. 

History and Physical

The medical history will likely reveal excessive consumption of vitamin A-rich foods, supplements, or oral retinoid medications. Symptoms include blurred vision, headaches, dry skin, hair loss, fatigue, and bone pain. Typical physical examination findings may include dryness of the conjunctiva and mucous membranes, scaly skin, alopecia, papilledema, bone tenderness, and hepatomegaly. 

Patients with a history of using topical vitamin A derivatives will likely exhibit localized skin peeling and erythema, but systemic signs and symptoms are not expected. 


A patient's history and physical examination findings guide the selection of diagnostic studies. Patients with persistent headaches while taking vitamin A medications should be evaluated for increased intracranial pressure and pseudotumor cerebri syndrome.

Laboratory findings obtained during assessing patients with vitamin A toxicity can reveal several abnormalities, a few of which are mentioned below.

Serum vitamin A levels: The serum vitamin A levels exceed 80 mcg/dL.

Liver function tests: Elevated levels of alanine transaminase (ALT), aspartate transaminase (AST), and alkaline phosphatase (ALP) indicate potential hepatic damage or inflammation.

Serum lipids: Increased levels of triglycerides and cholesterol are observed.

Hematological abnormalities: The identified abnormalities in the blood include leukocytosis, thrombocytopenia, and anemia.

Bone markers: Increased levels of ALP are associated with bone turnover.

Renal function: Elevations of blood urea nitrogen and creatinine occur.

Electrolyte imbalances: Alterations in electrolyte levels, such as sodium, potassium, and calcium occur.

Some patients require laboratory testing to monitor their condition. Individuals taking isotretinoin should undergo regular lipid level checks.[27] Elevations in liver enzymes are usually mild and reversible, although ALT and AST may need to be monitored based on the dosage and any comorbidities the patient may have.[28]

Women of childbearing age must have 2 negative pregnancy tests, conducted 30 days apart, before initiating isotretinoin treatment. Additional testing during and immediately after discontinuing the treatment is also necessary.[29] 

Free T4 should be monitored both before and during treatment with bexarotene.[30] In addition, baseline fasting serum lipid levels should be measured at treatment initiation and then every 1 to 2 weeks during therapy until they stabilize.

Patients with a history of kidney disease and undergoing etretinate therapy should regularly monitor their renal function throughout the treatment course.[17]

Treatment / Management

The treatment of systemic vitamin A toxicity includes discontinuing vitamin A intake, providing supportive care, and managing patient symptoms.

The management of skin irritation caused by topical retinoids involves reducing the volume and frequency of applications while increasing the use of emollients. Patients can be reassured that this adverse effect will likely improve with the continued use of the skincare products.

Acute retinoid toxicity is rare, but in documented cases, recovery is typically rapid upon discontinuation of the medication.[31] The sources of excess vitamin A intake, including dietary supplements and medications, must be identified as a primary step. Furthermore, healthcare professionals should recommend avoiding foods rich in preformed vitamin A to patients, such as liver and fortified products, until the toxicity resolves.

Supportive care involves close monitoring of the patient's condition, including vital signs and overall health status. Severe cases may necessitate hospital admission. Hypotension can be managed with fluid administration, and hypercalcemia can be treated with calcitonin and corticosteroids. When there is evidence of hepatic damage, liver function tests can assess the extent of the injury and guide further management decisions.

Patients with dry or peeling skin are advised to use moisturizers or emollients to alleviate discomfort and facilitate skin healing. For patients experiencing dry eyes, artificial tears and lubricating eye drops, including those containing methylcellulose, can be beneficial. 

The treatment of medication-induced chronic toxicity depends on the specific drug and its adverse effects. In cases where oral retinoids can lead to an elevation of the fasting triglyceride level to 800 mcg/dL or higher, options such as discontinuation, dose reduction, or the addition of lipid-lowering medication can be considered to prevent pancreatitis. Milder elevations can be monitored or treated similarly.

Patients experiencing toxicity from bexarotene can consider using a statin or fibrate concurrently to manage retinoid-induced hyperlipidemia and lower the risk of pancreatitis. Therapy may need to be discontinued if values remain elevated despite intervention and exceed 3 times the upper limit of normal.[32]

Patients diagnosed with pseudotumor cerebri syndrome should discontinue using vitamin A medications and might need acetazolamide to lower the intracranial pressure.[15]

Teratogenic malformations result in permanent damage, and the necessary supportive or surgical care varies based on the affected organ system.

Differential Diagnosis

When assessing the differential diagnosis of hypervitaminosis A, it is crucial to exclude other conditions that might manifest with similar symptoms, some of which are listed below.

Acute liver injury: Viral hepatitis, alcohol use, or drug toxicity.

Hypercalcemia: Hyperparathyroidism, malignancy, or excessive calcium and vitamin D intake.

Hypothyroidism: Primary thyroid disorders or medications.

Chronic renal failure: Diabetes, hypertension, glomerulonephritis, or polycystic kidney disease.

Central nervous system: Headache, nausea, and vomiting may be symptoms of pseudotumor cerebri and are not always caused by vitamin A toxicity.

Dermatological conditions: Exfoliative dermatitis and other skin conditions.

Nonspecific symptoms: The nonspecific symptoms, including skin rashes, joint pain, fatigue, and renal and liver abnormalities, can also indicate conditions such as systemic lupus erythematosus and may not solely point to vitamin A toxicity.


The prognosis of hypervitaminosis A depends on the severity of the condition and the duration of exposure to high levels of vitamin A. In most patients who discontinue the source of excess vitamin A, toxicity symptoms gradually reverse, and complete recovery is expected. Symptoms such as dry skin, headache, and nausea typically improve within a few weeks or months with no long-term complications.

However, severe cases can have serious consequences. Prolonged and excessive vitamin A intake can result in significant organ damage, including the liver, bones, central nervous system, and skin. Liver fibrosis or cirrhosis may be irreversible. Bone abnormalities, such as reduced bone density or fractures, may persist even after discontinuing vitamin A intake. In cases of pseudotumor cerebri, visual impairment may be permanent. The prognosis depends on the extent of organ damage and the promptness of medical intervention.


Complications of vitamin A toxicity include those listed below. 

Acute toxicity: Nausea, vomiting, headache, dizziness, irritability, blurred vision, and intracranial hypertension

Chronic toxicity: Dry, itchy skin, hair loss, bone and joint pain, fatigue, anorexia, and weight loss

Teratogenic effects: Craniofacial abnormalities, central nervous system malformations, and cardiovascular malformations

Hepatic toxicity: Hepatomegaly, elevated liver enzymes, jaundice, fibrosis, and cirrhosis

Skeletal abnormalities: Increased bone resorption, decreased bone formation, osteoporosis, fractures, and bone pain

Hematological disturbances: Leukocytosis, anemia, and thrombocytopenia

Central nervous system: Pseudotumor cerebri, with symptoms of headache, visual disturbances, and papilledema

Deterrence and Patient Education

Patient education regarding vitamin A toxicity is a shared responsibility among healthcare professionals, including physicians, advanced care practitioners, registered dietitians, nurses, and pharmacists. The significance of maintaining a balanced diet that includes essential vitamins and minerals is emphasized during routine medical appointments. Information regarding dietary sources of vitamin A, such as liver, fish, eggs, dairy products, and colorful fruits and vegetables, is provided to patients. Clinicians should advise patients about their recommended daily vitamin A intake according to their age, sex, and overall health.

Pharmacists provide information about both over-the-counter and prescription drugs containing vitamin A or its derivatives, including retinoids. They can elucidate the proper usage and potential adverse effects of these medications, underscoring the significance of adhering to the recommended dosage and treatment duration.

Obstetricians and other clinicians responsible for caring for women of childbearing age are responsible for educating them about the risks associated with excessive vitamin A intake from supplements or medications during pregnancy and the potential for teratogenic effects. 

If clinicians suspect toxicity, they should communicate the possible complications to patients and recommend discontinuing sources of vitamin A. This may involve dietary modifications and adjustments to medication and supplement usage.

Pearls and Other Issues

Teratogenicity is the most significant adverse effect of vitamin A toxicity. To mitigate this risk, patients should be counseled to avoid consuming more than the recommended amount of supplemental vitamin A during pregnancy. Most other adverse effects, such as skin irritation, dryness, and increased intracranial pressure, typically resolve when vitamin A intake or application is reduced or discontinued. Elevated triglycerides, cholesterol, or transaminases generally show improvement even with the continued use of the medication. Nevertheless, these levels should be closely monitored, and treatment should be discontinued if elevations persist or worsen.

Enhancing Healthcare Team Outcomes

Many individuals regularly consume substantial amounts of vitamins and supplements, often assuming they are safe due to their over-the-counter availability. However, poison control centers receive thousands of calls yearly related to vitamin overdoses and potential toxicity. An interprofessional team can collaborate to educate the public about these risks.

Healthcare professionals, including physicians, nurses, and pharmacists, must possess a comprehensive skill set to address vitamin A toxicity effectively. Pharmacists are critical in disseminating vitamin safety information to the public, advocating for a balanced, healthy diet over supplement reliance. They also instruct consumers about the vitamin A content in both over-the-counter and prescription medications. The nursing staff encourages patients to consume a healthy diet and refrain from taking vitamin A supplements unless advised by their medical provider. Primary care physicians should collaborate with nurses and pharmacists to ensure that patients maintain safe levels of vitamin A intake from dietary sources, supplements, and medications. 

Pregnancy is an absolute contraindication for isotretinoin therapy. Despite this, patients may still take other retinoid medications and supplements that have teratogenic effects. The nursing and medical staff, along with obstetricians and clinicians, are responsible for obtaining and coordinating patients' medication history, ensuring thorough documentation and periodic review of all medications, vitamins, and supplements. Patients should be informed about the teratogenic risks associated with excessive vitamin A intake and provided with guidance on the maximum recommended dosages during pregnancy.

By combining these skills, strategic approaches, shared responsibilities, effective communication, and seamless care coordination, healthcare professionals can deliver patient-centered care, optimize outcomes, enhance patient safety, and improve overall interprofessional team performance when managing vitamin A toxicity.

Review Questions


Hunt JR. Teratogenicity of high vitamin A intake. N Engl J Med. 1996 May 02;334(18):1197. [PubMed: 8602195]
Strobel M, Tinz J, Biesalski HK. The importance of beta-carotene as a source of vitamin A with special regard to pregnant and breastfeeding women. Eur J Nutr. 2007 Jul;46 Suppl 1:I1-20. [PubMed: 17665093]
Bastos Maia S, Rolland Souza AS, Costa Caminha MF, Lins da Silva S, Callou Cruz RSBL, Carvalho Dos Santos C, Batista Filho M. Vitamin A and Pregnancy: A Narrative Review. Nutrients. 2019 Mar 22;11(3) [PMC free article: PMC6470929] [PubMed: 30909386]
Penniston KL, Tanumihardjo SA. The acute and chronic toxic effects of vitamin A. Am J Clin Nutr. 2006 Feb;83(2):191-201. [PubMed: 16469975]
Lammer EJ, Chen DT, Hoar RM, Agnish ND, Benke PJ, Braun JT, Curry CJ, Fernhoff PM, Grix AW, Lott IT. Retinoic acid embryopathy. N Engl J Med. 1985 Oct 03;313(14):837-41. [PubMed: 3162101]
Lagacé M, Oskoui M, Myers K. Not a Benign Vitamin: Infant with Vitamin A Toxicity and Acute Intracranial Hypertension. Can J Neurol Sci. 2022 Dec 12;:1-2. [PubMed: 36503562]
Sauvant P, Féart C, Atgié C. Vitamin A supply to mothers and children: challenges and opportunities. Curr Opin Clin Nutr Metab Care. 2012 May;15(3):310-4. [PubMed: 22406743]
Arlappa N. Vitamin A supplementation policy: A shift from universal to geographical targeted approach in India considered detrimental to health and nutritional status of under 5 years children. Eur J Clin Nutr. 2023 Jan;77(1):1-6. [PMC free article: PMC8959797] [PubMed: 35347255]
Ball MD, Furr HC, Olson JA. Acyl coenzyme A:retinol acyltransferase activity and the vitamin A content of polar bear (Ursus maritimus) liver. Comp Biochem Physiol B. 1986;84(4):513-7. [PubMed: 3757481]
Senoo H, Imai K, Mezaki Y, Miura M, Morii M, Fujiwara M, Blomhoff R. Accumulation of vitamin A in the hepatic stellate cell of arctic top predators. Anat Rec (Hoboken). 2012 Oct;295(10):1660-8. [PubMed: 22907891]
Mahoney CP, Margolis MT, Knauss TA, Labbe RF. Chronic vitamin A intoxication in infants fed chicken liver. Pediatrics. 1980 May;65(5):893-7. [PubMed: 7189278]
Horowitz BZ. Did hypervitaminosis A have a role in Mawson's ill-fated Antarctic exploration? Clin Toxicol (Phila). 2022 Nov;60(11):1277-1281. [PubMed: 36286587]
Scheven BA, Hamilton NJ. Retinoic acid and 1,25-dihydroxyvitamin D3 stimulate osteoclast formation by different mechanisms. Bone. 1990;11(1):53-9. [PubMed: 2331432]
Genaro Pde S, Martini LA. Vitamin A supplementation and risk of skeletal fracture. Nutr Rev. 2004 Feb;62(2):65-7. [PubMed: 15080368]
Chisholm JT, Abou-Jaoude MM, Hessler AB, Sudhakar P. Pseudotumor Cerebri Syndrome with Resolution After Discontinuing High Vitamin A Containing Dietary Supplement: Case Report and Review. Neuroophthalmology. 2018 Jun;42(3):169-175. [PMC free article: PMC5958954] [PubMed: 29796052]
Sherman SI, Gopal J, Haugen BR, Chiu AC, Whaley K, Nowlakha P, Duvic M. Central hypothyroidism associated with retinoid X receptor-selective ligands. N Engl J Med. 1999 Apr 08;340(14):1075-9. [PubMed: 10194237]
Cribier B, Welsch M, Heid E. Renal impairment probably induced by etretinate. Dermatology. 1992;185(4):266-8. [PubMed: 1477420]
Koo J, Nguyen Q, Gambla C. Advances in psoriasis therapy. Adv Dermatol. 1997;12:47-72; discussion 73. [PubMed: 8973735]
Duvic M, Martin AG, Kim Y, Olsen E, Wood GS, Crowley CA, Yocum RC., Worldwide Bexarotene Study Group. Phase 2 and 3 clinical trial of oral bexarotene (Targretin capsules) for the treatment of refractory or persistent early-stage cutaneous T-cell lymphoma. Arch Dermatol. 2001 May;137(5):581-93. [PubMed: 11346336]
Nollevaux MC, Guiot Y, Horsmans Y, Leclercq I, Rahier J, Geubel AP, Sempoux C. Hypervitaminosis A-induced liver fibrosis: stellate cell activation and daily dose consumption. Liver Int. 2006 Mar;26(2):182-6. [PubMed: 16448456]
Bigby M. Does isotretinoin increase the risk of depression? Arch Dermatol. 2008 Sep;144(9):1197-9; discussion 1234-5. [PubMed: 18794466]
Rothman KJ, Moore LL, Singer MR, Nguyen US, Mannino S, Milunsky A. Teratogenicity of high vitamin A intake. N Engl J Med. 1995 Nov 23;333(21):1369-73. [PubMed: 7477116]
Marshall H, Studer M, Pöpperl H, Aparicio S, Kuroiwa A, Brenner S, Krumlauf R. A conserved retinoic acid response element required for early expression of the homeobox gene Hoxb-1. Nature. 1994 Aug 18;370(6490):567-71. [PubMed: 7914354]
Inkeles SB, Connor WE, Illingworth DR. Hepatic and dermatologic manifestations of chronic hypervitaminosis A in adults. Report of two cases. Am J Med. 1986 Mar;80(3):491-6. [PubMed: 2937294]
Chen G, Weiskirchen S, Weiskirchen R. Vitamin A: too good to be bad? Front Pharmacol. 2023;14:1186336. [PMC free article: PMC10239981] [PubMed: 37284305]
Moise AR, Noy N, Palczewski K, Blaner WS. Delivery of retinoid-based therapies to target tissues. Biochemistry. 2007 Apr 17;46(15):4449-58. [PMC free article: PMC2562735] [PubMed: 17378589]
Goldsmith LA, Bolognia JL, Callen JP, Chen SC, Feldman SR, Lim HW, Lucky AW, Reed BR, Siegfried EC, Thiboutot DM, Wheeland RG., American Academy of Dermatology. American Academy of Dermatology Consensus Conference on the safe and optimal use of isotretinoin: summary and recommendations. J Am Acad Dermatol. 2004 Jun;50(6):900-6. [PubMed: 15153892]
Sammartano A, Bertoncini L, Barbuti A, Ippolito L. A suspected hypervitaminosis A. Acta Biomed. 2023 Jun 14;94(3):e2023098. [PMC free article: PMC10308465] [PubMed: 37326274]
Cook MK, Perche PO, Feldman SR. The use of oral vitamin A in acne management: a review. Dermatol Online J. 2022 Oct 15;28(5) [PubMed: 36809126]
Gniadecki R, Assaf C, Bagot M, Dummer R, Duvic M, Knobler R, Ranki A, Schwandt P, Whittaker S. The optimal use of bexarotene in cutaneous T-cell lymphoma. Br J Dermatol. 2007 Sep;157(3):433-40. [PubMed: 17553039]
Nagai K, Hosaka H, Kubo S, Nakabayashi T, Amagasaki Y, Nakamura N. Vitamin A toxicity secondary to excessive intake of yellow-green vegetables, liver and laver. J Hepatol. 1999 Jul;31(1):142-8. [PubMed: 10424294]
Wiegand UW, Chou RC. Pharmacokinetics of acitretin and etretinate. J Am Acad Dermatol. 1998 Aug;39(2 Pt 3):S25-33. [PubMed: 9703120]

Disclosure: Jazmine Olson declares no relevant financial relationships with ineligible companies.

Disclosure: Muhammad Atif Ameer declares no relevant financial relationships with ineligible companies.

Disclosure: Amandeep Goyal declares no relevant financial relationships with ineligible companies.

Copyright © 2024, StatPearls Publishing LLC.

This book is distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0) ( http://creativecommons.org/licenses/by-nc-nd/4.0/ ), which permits others to distribute the work, provided that the article is not altered or used commercially. You are not required to obtain permission to distribute this article, provided that you credit the author and journal.

Bookshelf ID: NBK532916PMID: 30422511


  • PubReader
  • Print View
  • Cite this Page

Related information

  • PMC
    PubMed Central citations
  • PubMed
    Links to PubMed

Similar articles in PubMed

See reviews...See all...

Recent Activity

Your browsing activity is empty.

Activity recording is turned off.

Turn recording back on

See more...