Fixed Drug Eruptions



The term fixed drug eruption (FDE) describes the development of one or more annular or oval erythematous patches as a result of systemic exposure to a drug; these reactions normally resolve with hyperpigmentation and may recur at the same site with reexposure to the drug. Repeated exposure to the offending drug may cause new lesions to develop in addition to "lighting up" the older hyperpigmented lesions.

Adverse reactions to medications are common and often manifest as a cutaneous eruption. Drug-induced cutaneous disorders frequently display a characteristic clinical morphology such as morbilliform exanthem, urticaria, hypersensitivity syndrome, pseudolymphoma, photosensitivity, pigmentary changes, acute generalized exanthematous pustulosis, lichenoid dermatitis, vasculitis, Stevens-Johnson syndrome, or fixed drug eruption.

Several variants of fixed drug eruption have been described, based on their clinical features and the distribution of the lesions.[1, 2, 3, 4, 5, 6, 7] These include the following:

Also see the following related Medscape articles:


Although the exact mechanism is unknown, recent research suggests a cell-mediated process that initiates both the active and quiescent lesions. The process may involve an antibody-dependent, cell-mediated cytotoxic response.[9] CD8+ effector/memory T cells play an important role in reactivation of lesions with re-exposure to the offending drug.[10, 11]

The offending drug is thought to function as a hapten that preferentially binds to basal keratinocytes, leading to an inflammatory response.[12] Through liberation of cytokines such as tumor necrosis factor-alpha, keratinocytes may locally up-regulate expression of the intercellular adhesion molecule-1 (ICAM1).[13] The up-regulated ICAM1 has been shown to help T cells (CD4 and CD8) migrate to the site of an insult.[14, 15]

The newly arriving and residential CD8 cells likely perpetuate tissue damage by their production of the inflammatory cytokines interferon-gamma and tumor necrosis factor-alpha. CD8 cells isolated from active lesions have also been shown to express alpha E beta 7, a ligand for E-cadherin, which may further contribute to the lymphocyte’s ability to localize to the epidermis. Other cell surface molecules, such as CLA/alpha4beta1/CD4a, that bind E-selectin/vascular cellular adhesion molecule-2/ICAM1 help to further attract CD8 cells to the area.[9]

Changes in cell surface markers allow vascular endothelium to select CD4 cells for migration into active lesions. These regulatory CD4 cells likely produce interleukin 10, which has been shown to help suppress immune function, resulting in a resting lesion.[9] As the inflammatory response dissipates, interleukin 15 expression from keratinocytes is thought to help ensure the survival of CD8 cells, helping them fulfill their effector memory phenotypes. Thus, when reexposure to the drug occurs, a more rapid response develops in the exact location of any prior lesions.[9]


The major categories of causative agents of fixed drug eruption include antibiotics, antiepileptics, nonsteroidal anti-inflammatory agents, sildenafil, and phenothiazines, although numerous other agents and certain foods such as cashews and licorice have also been reported as causative agents. Ingestion of the causative agent may occur via any route, including oral, rectal, or intravenous.[16, 17]

Certain classes of drugs with cross-reactions within a class have been reported to elicit a fixed drug eruption with quinolones[18] and with nonsteroidal anti-inflammatory agents.[19] In some patients, the reaction may be to a dye rather than the active ingredient.[20] Fixed drug eruption may rarely be related to foods, including residual antibiotics in meat products and quinine contained in tonic water.[21, 22]

While fixed drug eruptions are uncommon with general anesthesia, propofol has been implicated in causing a drug eruption on the penis.[23]

The most common cause is trimethoprim-sulfamethoxazole.[3, 24] Other substances implicated to cause fixed drug eruptions are as follows[1, 12, 16, 25, 5, 26, 27, 28, 29, 30, 31, 32, 33, 34, 35, 36] :

Table. Substances Implicated in Fixed Drug Eruptions

View Table

See Table



United States

The prevalence of drug eruptions has been reported to range from 2-5% for inpatients and greater than 1% for outpatients.[37] Fixed drug eruptions may account for as much as 16-21% of all cutaneous drug eruptions. The actual frequency may be higher than current estimates, owing to the availability of a variety of over-the-counter medications and nutritional supplements that are known to elicit fixed drug eruptions.


The international prevalence is variable but is likely similar to that in the United States. Most studies report fixed drug eruptions to be the second or third most common skin manifestation of adverse drug events.[38]


Fixed drug eruptions have no known racial predilection. A genetic susceptibility to developing a fixed drug eruption with an increased incidence of HLA-B22 is possible.[39, 40]


One large study of 450 patients revealed a male-to-female ratio of 1:1.1 for fixed drug eruptions.[1]


Fixed drug eruptions have been reported in patients as young as 1.5 years and as old as 87 years. The mean age at presentation is 30.4 years in males and 31.3 years in females.[1]


The prognosis is very good, and an uneventful recovery should be expected. No deaths due to fixed drug eruption have been reported. Residual hyperpigmentation is very common, but this is less likely with the nonpigmenting variant.

Widespread lesions may initially mimic toxic epidermal necrolysis, but they have a benign clinical course.[41] Again, localized hyperpigmentation is a common complication, but pain, infection, and, rarely, hypopigmentation, also may occur.[1]

Patient Education

Patients should be counseled on medication avoidance and possible cross-reactions of similar medications. Patients should notify their physicians of all drug allergies they have experienced.


The initial eruption is often solitary and frequently located on the lip or genitalia. Rarely, the eruption may be intraoral. Other common locations of the initial lesion are the hip, lower back/sacrum, or proximal extremity. With the initial fixed drug eruption attack, a delay of up to 2 weeks may occur from the initial exposure to the drug to the development of the skin lesion.[42] Skin lesions develop over a period of hours but require days to become necrotic. Lesions may persist from days to weeks and then fade slowly to residual oval hyperpigmented patches.

Subsequent reexposure to the medication results in a reactivation of the site, with inflammation occurring within 30 minutes to 16 hours.[43] The reactivation of old lesions also may be associated with the development of new lesions at other sites.

Patients may not be cognizant that a drug, nutritional supplement, over-the-counter medication, or, rarely, food (eg, fruits, nuts) triggered the skin problem. They may be convinced that an insect, particularly a spider, may be the culprit. A careful history is required to elicit the fact that a drug has been taken and is temporally related to the onset of the eruption. Medications taken episodically, such as pain relievers, antibiotics, or laxatives, are often to blame. When able to be identified, patients often report ingestion of one the following types of medications[16] :

Local symptoms may include pruritus, burning, and pain.[1] Systemic symptoms are uncommon, but fever, malaise, nausea, diarrhea, abdominal cramps, anorexia, and dysuria have been reported.[43, 16]

Further questioning may reveal prior episodes of fixed drug eruption, atopic disease, or other past drug reactions. Family history may render a history of atopy, drug reactions, or diabetes mellitus.[1]

Several cases of fixed drug eruption on the genitalia have been reported in patients who were not ingesting the drug but whose sexual partner was taking the offending drug and the patient was exposed to the drug through sexual contact.[44, 45, 46]

Physical Examination

The most common clinical manifestation is the pigmenting fixed drug eruption, which usually manifests as round or oval, sharply demarcated erythematous/edematous plaques located on the lip, hip, sacrum, or genitalia.[2] These erythematous patches or plaques gradually fade with residual hyperpigmentation (see images below). The center of the patch may blister or become necrotic. Other less common variants may manifest as lesions resembling erythema multiforme, toxic epidermal necrolysis, eczema, urticaria, a linear pattern following Blaschko lines, bullous lesions, a migrating eruption, or a nonpigmenting form with no postinflammatory hyperpigmentation.[3]  Pseudoephedrine,[47] piroxicam,[48] cotrimoxazole,[49] sorafenib,[50] and tadalafil[51] have all been reported to cause the nonpigmenting form of this condition.

View Image

Targetoid fixed drug eruption on the abdomen of a child.

View Image

Hyperpigmented fixed drug eruption on the hip of an adult.

View Image

Vesicular fixed drug eruption on the glans penis.

View Image

Multiple hyperpigmented fixed drug eruptions on the trunk.

View Image

Hyperpigmented fixed drug eruption on the right side of the upper lip.

Initially, a single lesion or a few lesions develop, but, with reexposure, additional lesions occur. The vast majority of patients present with 1-30 lesions, ranging in size of 0.5-5 cm, but reports of lesions greater than 10 cm have been published. Lesions may be generalized. The most common reported site is the lips, and these may be seen in up to half of all cases.[1]

Medications may also follow a site-specific eruption pattern. For example, trimethoprim-sulfamethoxazole (Bactrim) has been shown to favor the genital region (especially in males) and naproxen and the oxicams involve the lips.[2]

Resting/inactive lesions tend to appear as round or oval, gray, hyperpigmented macules.

Upon reexposure, the resting hyperpigmented macules activate, developing a violaceous center encircled by concentric rings of erythema. Re-administration of the medication poses the risk of increased pigmentation, size, and number of lesions.

Individuals with darker pigmentation may develop postinflammatory hypopigmented macules once the lesions have resolved.[12]


Hyperpigmentation is the most likely complication of a fixed drug eruption (FDE). The potential for infection exists in the setting of multiple, eroded lesions. Generalized eruptions have been reported following topical and oral provocation testing.[16, 52]

Laboratory Studies

Blood studies are not useful for the diagnosis of fixed drug eruption (FDE), although eosinophilia is common with drug eruptions.

Other Tests

Patch testing and oral provocation have been used to identify the suspected agent and check for cross-sensitivities to medications.[53, 54, 55, 56] A refractory period has been reported in fixed drug eruption; therefore, a delay before and between patch testing and oral provocation is recommended. One study used an 8-week time window after lesion resolution and between tests, which yielded positive results.[57] Patch testing must be performed on a previously involved site; otherwise, a false-negative result is likely.[54] Some locations may be inappropriate for patch testing; thus, clinical discretion is advised. Once patch testing is complete, oral provocation should follow, with the least likely culprits and the negative patch test agents first, followed by more likely causes. Oral provocation is thought to be the only reliable way to diagnose fixed drug eruption.

Patch testing is particularly efficacious in identifying a putative cause of the reaction when nonsteroidal anti-inflammatory agents are suspected, but patch testing is not helpful in discerning reactions to antibiotics and allopurinol.[58]


Skin biopsy is the diagnostic procedure of choice.

Histologic Findings

Histological examination of inflammatory/acute lesions shows an interface dermatitis with vacuolar change and Civatte bodies[12] (see the image below).

View Image

Acute interface dermatitis with prominent vacuolar change and individual necrotic keratinocytes within the epidermis (X10).

The overall pattern may mimic that seen in erythema multiforme. Dyskeratosis and individual necrotic keratinocytes within the epidermis may be a prominent feature (see the image below).

View Image

Interface dermatitis, vacuolar change, necrotic keratinocytes, and incontinent pigment in the dermis (X40).

On occasion, the lymphocytic infiltrate can be prominent enough to obscure the dermoepidermal junction. Spongiosis, dermal edema, eosinophils, and occasional neutrophils may be present. Pigmentary incontinence within the papillary dermis is a characteristic feature and may be the only feature seen in older, noninflamed lesions. Chronic or inactive lesions may also show mild acanthosis, hyperkeratosis, and relatively few inflammatory cells.

Medical Care

The main goal of treatment is to identify the causative agent and avoid it. Treatment for fixed drug eruptions (FDEs) otherwise is symptomatic. Systemic antihistamines and topical corticosteroids may be all that are required. In cases in which infection is suspected, antibiotics and proper wound care are advised. Desensitization to medications has been reported in the literature, but this should be avoided unless no substitutes exist.[59] In severe cases, cyclosporine has been used.[60]


Consultation with a dermatologist is warranted if the diagnosis is in doubt. If patch testing is needed to determine which drug may be involved, a dermatologist with such experience may be required. If Stevens-Johnson syndrome or toxic epidermal necrolysis is suspected, hospitalization and possible referral to the intensive care unit or burn unit may be appropriate.


A regular diet is usually acceptable. However, food may be an exacerbating factor; reactivation has been reported with cashews, liquorice, lentils, and strawberries.[12, 30, 33]


Generally, no limits on activities are imposed. Multiple studies have sited male genital lesions occurring following intercourse with female partners taking trimethoprim-sulfamethoxazole.[61] Therefore, patients may consider avoiding sexual activity while a partner is taking a medication that has resulted in a prior fixed drug eruption. If open lesions are present, general wound care precautions are recommended.


Avoid the offending drug. Patch testing may be used to help identify agents that pose a risk of cross-sensitivity.[62]

Medication Summary

Lesions of fixed drug eruption resolve spontaneously with avoidance of the inciting drug. Additional medications should be used to relieve symptoms associated with the condition. Generally, an oral antihistamine (eg, hydroxyzine) and a topical corticosteroid may be sufficient. The use of corticosteroids may interfere with later diagnostic provocation testing. Hyperpigmentation may take many months to resolve. Incontinent pigment in the dermis responds poorly to topical bleaching agents such as hydroquinones.

What is a fixed drug eruption (FDE)?What are the variants of fixed drug eruptions (FDE)?What is the pathophysiology of fixed drug eruptions (FDE)?What are causative agents of fixed drug eruptions (FDE)?How common are fixed drug eruptions (FDE) in the US?What is the international prevalence of fixed drug eruptions (FDE)?Do fixed drug eruptions (FDE) have a racial predilection?What are the sex-related demographics of fixed drug eruptions (FDE)?What are the age-related demographics of fixed drug eruptions (FDE)?What is the prognosis of fixed drug eruption (FDE)?What is involved in patient education for fixed drug eruptions (FDE)?What is the clinical history of fixed drug eruptions (FDE)?Which medications are associated with fixed drug eruptions (FDE)?What are the symptoms of fixed drug eruptions (FDE)?What is the clinical manifestation of fixed drug eruption (FDE)?What are common physical findings of fixed drug eruptions (FDE)?What are the complications of fixed drug eruptions (FDE)?What are the differential diagnoses for Fixed Drug Eruptions?Are blood studies useful in the workup of fixed drug eruptions (FDE)?What other tests are indicated in the workup of fixed drug eruptions (FDE)?What is the diagnostic procedure of choice for fixed drug eruptions (FDE)?What are histologic findings of fixed drug eruptions (FDE)?What is the main goal of treatment for fixed drug eruptions (FDE)?Which specialist consultations are recommended in the treatment of fixed drug eruptions (FDE)?What dietary recommendations are indicated in the treatment of fixed drug eruptions (FDE)?Should activity be restricted in the treatment of fixed drug eruptions (FDE)?What is involved in the prevention of fixed drug eruptions (FDE)?What is the medical therapy for fixed drug eruptions (FDE)?


David F Butler, MD, Former 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

Disclosure: Nothing to disclose.

Specialty Editors

Richard P Vinson, MD, Assistant Clinical Professor, Department of Dermatology, Texas Tech University Health Sciences Center, Paul L Foster School of Medicine; Consulting Staff, Mountain View Dermatology, PA

Disclosure: Nothing to disclose.

Jeffrey P Callen, MD, Professor of Medicine (Dermatology), Chief, Division of Dermatology, University of Louisville School of Medicine

Disclosure: Received honoraria from UpToDate for author/editor; Received royalty from Elsevier for book author/editor; Received dividends from trust accounts, but I do not control these accounts, and have directed our managers to divest pharmaceutical stocks as is fiscally prudent from Stock holdings in various trust accounts include some pharmaceutical companies and device makers for i inherited these trust accounts; for: Allergen; Celgene; Pfizer; 3M; Johnson and Johnson; Merck; Abbott Laboratories; AbbVie; Procter and Gamble; Amgen.

Chief Editor

Dirk M Elston, MD, Professor and Chairman, Department of Dermatology and Dermatologic Surgery, Medical University of South Carolina College of Medicine

Disclosure: Nothing to disclose.

Additional Contributors

Robert A Schwartz, MD, MPH, Professor and Head of Dermatology, Professor of Pathology, Professor of Pediatrics, Professor of Medicine, Rutgers New Jersey Medical School

Disclosure: Nothing to disclose.


Jordan R Ilse, MD Staff Physician, Scott and White Internal Medicine Residency Program, Scott and White Clinic, Texas A&M University College of Medicine

Jordan R Ilse, MD is a member of the following medical societies: American Medical Association and Texas Medical Association

Disclosure: Nothing to disclose.


  1. Mahboob A, Haroon TS. Drugs causing fixed eruptions: a study of 450 cases. Int J Dermatol. 1998 Nov. 37(11):833-8. [View Abstract]
  2. Ozkaya-Bayazit E. Specific site involvement in fixed drug eruption. J Am Acad Dermatol. 2003 Dec. 49(6):1003-7. [View Abstract]
  3. Ozkaya-Bayazit E, Bayazit H, Ozarmagan G. Drug related clinical pattern in fixed drug eruption. Eur J Dermatol. 2000 Jun. 10(4):288-91. [View Abstract]
  4. Fischer G. Vulvar fixed drug eruption. A report of 13 cases. J Reprod Med. 2007 Feb. 52(2):81-6. [View Abstract]
  5. Gupta S, Gupta S, Mittal A, David S. Oral fixed drug eruption caused by gabapentin. J Eur Acad Dermatol Venereol. 2009 Feb 19. [View Abstract]
  6. Katoulis AC, Bozi E, Kanelleas A, et al. Psoriasiform fixed drug eruption caused by nimesulide. Clin Exp Dermatol. 2009 Oct. 34(7):e360-1. [View Abstract]
  7. Srivastava R, Bihari M, Bhuvan J, Saad A. Fixed drug eruptions with intraoral presentation. Indian J Dent. 2015 Apr-Jun. 6 (2):103-6. [View Abstract]
  8. Fathallah N, Ben Salem C, Slim R, Boussofara L, Ghariani N, Bouraoui K. Acetaminophen-induced cellulitis-like fixed drug eruption. Indian J Dermatol. 2011 Mar. 56(2):206-8. [View Abstract]
  9. Teraki Y, Shiohara T. IFN-gamma-producing effector CD8+ T cells and IL-10-producing regulatory CD4+ T cells in fixed drug eruption. J Allergy Clin Immunol. 2003 Sep. 112(3):609-15. [View Abstract]
  10. Mizukawa Y, Shiohara T. Fixed drug eruption: a prototypic disorder mediated by effector memory T cells. Curr Allergy Asthma Rep. 2009 Jan. 9(1):71-7. [View Abstract]
  11. Shiohara T. Fixed drug eruption: pathogenesis and diagnostic tests. Curr Opin Allergy Clin Immunol. 2009 Aug. 9(4):316-21. [View Abstract]
  12. Weedon D. The lichenoid reaction pattern ('interface dermatitis'). Skin Pathology. 2nd ed. London, England: Churchill Livingstone; 2002. 42-43.
  13. Smoller BR, Luster AD, Krane JF, et al. Fixed drug eruptions: evidence for a cytokine-mediated process. J Cutan Pathol. 1991 Feb. 18(1):13-9. [View Abstract]
  14. Hindsen M, Christensen OB, Gruic V, Lofberg H. Fixed drug eruption: an immunohistochemical investigation of the acute and healing phase. Br J Dermatol. 1987 Mar. 116(3):351-60. [View Abstract]
  15. Shiohara T, Nickoloff BJ, Sagawa Y, Gomi T, Nagashima M. Fixed drug eruption. Expression of epidermal keratinocyte intercellular adhesion molecule-1 (ICAM-1). Arch Dermatol. 1989 Oct. 125(10):1371-6. [View Abstract]
  16. Sehgal VN, Srivastava G. Fixed drug eruption (FDE): changing scenario of incriminating drugs. Int J Dermatol. 2006 Aug. 45(8):897-908. [View Abstract]
  17. Choi SY, Suh JH, Park KY, Li K, Kim BJ, Seo SJ, et al. Fixed Drug Eruption Caused by Sildenafil Citrate. Ann Dermatol. 2017 Apr. 29 (2):247-248. [View Abstract]
  18. Sánchez-Morillas L, Rojas Pérez-Ezquerra P, González Morales ML, Mayorga C, González-Mendiola R, Laguna Martínez JJ. Fixed drug eruption due to norfloxacin and cross-reactivity with other quinolones. Allergol Immunopathol (Madr). 2012 Jan 20. [View Abstract]
  19. Pérez-Calderón R, Gonzalo-Garijo MA, Pérez-Rangel I, Sánchez-Vega S, Zambonino MA. Fixed drug eruption due to nabumetone in a patient with previous fixed drug eruptions due to naproxen. J Investig Allergol Clin Immunol. 2011. 21(2):153-4. [View Abstract]
  20. Leleu C, Boulitrop C, Bel B, Jeudy G, Vabres P, Collet E. Quinoline Yellow dye-induced fixed food-and-drug eruption. Contact Dermatitis. 2013 Mar. 68(3):187-8. [View Abstract]
  21. Lim WS, Kim DH, Jin SY, Choi YS, Lee SH, Huh HJ, et al. A case of fixed drug eruption due to doxycycline and erythromycin present in food. Allergy Asthma Immunol Res. 2013 Sep. 5(5):337-9. [View Abstract]
  22. Ohira A, Yamaguchi S, Miyagi T, et al. Fixed eruption due to quinine in tonic water: a case report with high-performance liquid chromatography and ultraviolet A analyses. J Dermatol. 2013 Aug. 40(8):629-31. [View Abstract]
  23. Allchurch LG, Crilly H. Fixed drug eruption to propofol. Anaesth Intensive Care. 2014 Nov. 42 (6):777-81. [View Abstract]
  24. Centers for Disease Control and Prevention. Fixed drug eruption associated with sulfonamides sold in Latino grocery stores - Greater Washington, DC, area, 2012-2013. MMWR Morb Mortal Wkly Rep. 2013 Nov 22. 62(46):914-6. [View Abstract]
  25. Lopez Abad R, Iriarte Sotes P, Castro Murga M, Gracia Bara MT, Sesma Sanchez P. Fixed drug eruption induced by phenylephrine: a case of polysensitivity. J Investig Allergol Clin Immunol. 2009. 19(4):322-3. [View Abstract]
  26. Ghosh SK, Bandyopadhyay D. Clopidogrel-induced fixed drug eruption. J Eur Acad Dermatol Venereol. 2009 Jan 20. [View Abstract]
  27. Oyama N, Kaneko F. Solitary fixed drug eruption caused by finasteride. J Am Acad Dermatol. 2009 Jan. 60(1):168-9. [View Abstract]
  28. Knapp CF 3rd, Cooke ER, Sheehan DJ. Bullous fixed drug eruption caused by flecainide. J Am Acad Dermatol. 2009 Feb. 60(2):e3. [View Abstract]
  29. Ozkaya E, Mirzoyeva L, Jhaish MS. Ceftriaxone-induced fixed drug eruption: first report. Am J Clin Dermatol. 2008. 9(5):345-7. [View Abstract]
  30. Fukushima S, Kidou M, Ihn H. Fixed food eruption caused by cashew nut. Allergol Int. 2008 Sep. 57(3):285-7. [View Abstract]
  31. Takahama H. A fixed drug eruption that developed cross-sensitivity among amide local anaesthetics, including mepivacaine hydrochloride, lidocaine hydrochloride and propitocaine hydrochloride. J Eur Acad Dermatol Venereol. 2008 Nov. 22(11):1400-1. [View Abstract]
  32. Bohm I, Medina J, Prieto P, Block W, Schild HH. Fixed drug eruption induced by an iodinated non-ionic X-ray contrast medium: a practical approach to identify the causative agent and to prevent its recurrence. Eur Radiol. 2007 Feb. 17(2):485-9. [View Abstract]
  33. Benomar S, Ismaili N, Koufane J, Senouci K, Hassam B. [Fixed food eruption caused by liquorice.]. Ann Dermatol Venereol. 2010 Feb. 137(2):121-123. [View Abstract]
  34. Orellana-Barrios M, Medrano Juarez R, Patel NJ. Fixed drug eruption associated with aspirin. BMJ Case Rep. 2018 Mar 17. 2018:[View Abstract]
  35. Zaouak A, Ben Brahim E, Ben Tanfous A, Koubaa W, Sahnoun R, Hammami H, et al. Mucosal fixed drug eruption due to mefenamic acid: Report of a case and a review. Therapie. 2018 Feb 15. [View Abstract]
  36. Özkaya E. Changing trends in inducer drugs of fixed drug eruption: a 20-year cross-sectional study from Turkey. J Dtsch Dermatol Ges. 2018 Apr. 16 (4):474-476. [View Abstract]
  37. Krahenbuhl-Melcher A, Schlienger R, Lampert M, Haschke M, Drewe J, Krahenbuhl S. Drug-related problems in hospitals: a review of the recent literature. Drug Saf. 2007. 30(5):379-407. [View Abstract]
  38. Lee AY. Fixed drug eruptions. Incidence, recognition, and avoidance. Am J Clin Dermatol. 2000 Sep-Oct. 1(5):277-85. [View Abstract]
  39. Pellicano R, Ciavarella G, Lomuto M, Di Giorgio G. Genetic susceptibility to fixed drug eruption: evidence for a link with HLA-B22. J Am Acad Dermatol. 1994 Jan. 30(1):52-4. [View Abstract]
  40. Pellicano R, Lomuto M, Ciavarella G, Di Giorgio G, Gasparini P. Fixed drug eruptions with feprazone are linked to HLA-B22. J Am Acad Dermatol. 1997 May. 36(5 Pt 1):782-4. [View Abstract]
  41. Baird BJ, De Villez RL. Widespread bullous fixed drug eruption mimicking toxic epidermal necrolysis. Int J Dermatol. 1988 Apr. 27(3):170-4. [View Abstract]
  42. Bolognia JL, Jorizzo JL, Rapini RP. Fixed drug eruptions. Dermatology. London, England: Mosby; 2003. 344-5.
  43. Freedberg IM, Eisen AZ, Wolff K, Austen KF, Goldsmith LA, Katz SI. Fixed drug eruptions. Fitzpatrick’s Dermatology in General Medicine. 6th ed. New York, NY: McGraw-Hill; 2003. 1333.
  44. Zawar V, Chuh A. Fixed drug reaction may be sexually induced. Int J Dermatol. 2006 Aug. 45(8):1003-4; author reply 1004. [View Abstract]
  45. Berger RE. Fixed drug eruption--a sexually inducible reaction?. J Urol. 2005 Jun. 173(6):1990. [View Abstract]
  46. Zawar V, Kirloskar M, Chuh A. Fixed drug eruption - a sexually inducible reaction?. Int J STD AIDS. 2004 Aug. 15(8):560-3. [View Abstract]
  47. Vidal C, Prieto A, Pérez-Carral C, Armisén M. Nonpigmenting fixed drug eruption due to pseudoephedrine. Ann Allergy Asthma Immunol. 1998 Apr. 80 (4):309-10. [View Abstract]
  48. Montoro J, Díaz M, Genís C, Lozano A, Bertomeu F. Non-pigmenting cutaneous-mucosal fixed drug eruption due to piroxicam. Allergol Immunopathol (Madr). 2003 Jan-Feb. 31 (1):53-5. [View Abstract]
  49. Rasi A, Khatami A. Unilateral non-pigmenting fixed drug eruption associated with cotrimoxazole. Dermatol Online J. 2006 Oct 31. 12 (6):12. [View Abstract]
  50. Tanabe K, Amoh Y, Mii S, Eto H, Iwamura M, Katsuoka K. Non-pigmenting fixed drug eruption induced by sorafenib. Acta Derm Venereol. 2010 May. 90 (3):307. [View Abstract]
  51. Das S, Das S, Chowdhury J, Bhanja DC. Non pigmenting mucosal fixed drug eruption due to tadalafil: A report of two cases. Indian Dermatol Online J. 2014 Apr. 5 (2):167-9. [View Abstract]
  52. Gonzalo-Garijo MA, de Argila D, Rodriguez-Nevado I. Generalized reaction after patch testing with metamizol. Contact Dermatitis. 2001 Sep. 45(3):180. [View Abstract]
  53. Lammintausta K, Kortekangas-Savolainen O. Oral challenge in patients with suspected cutaneous adverse drug reactions: findings in 784 patients during a 25-year-period. Acta Derm Venereol. 2005. 85(6):491-6. [View Abstract]
  54. Lammintausta K, Kortekangas-Savolainen O. The usefulness of skin tests to prove drug hypersensitivity. Br J Dermatol. 2005 May. 152(5):968-74. [View Abstract]
  55. Li PH, Watts TJ, Chung HY, Lau CS. Fixed Drug Eruption to Biologics and Role of Lesional Patch Testing. J Allergy Clin Immunol Pract. 2019 Jul 17. [View Abstract]
  56. Ben Fadhel N, Chaabane A, Ammar H, Ben Romdhane H, Soua Y, Chadli Z, et al. Clinical features, culprit drugs, and allergology workup in 41 cases of fixed drug eruption. Contact Dermatitis. 2019 Jul 10. [View Abstract]
  57. Zedlitz S, Linzbach L, Kaufmann R, Boehncke WH. Reproducible identification of the causative drug of a fixed drug eruption by oral provocation and lesional patch testing. Contact Dermatitis. 2002 Jun. 46(6):352-3. [View Abstract]
  58. Andrade P, Brinca A, Gonçalo M. Patch testing in fixed drug eruptions--a 20-year review. Contact Dermatitis. 2011 Oct. 65(4):195-201. [View Abstract]
  59. Kelso JM, Keating RM. Successful desensitization for treatment of a fixed drug eruption to allopurinol. J Allergy Clin Immunol. 1996 May. 97(5):1171-2. [View Abstract]
  60. Malviya N, Cyrus N, Vandergriff T, Mauskar M. Generalized bullous fixed drug eruption treated with cyclosporine. Dermatol Online J. 2017 Feb 15. 23 (2):[View Abstract]
  61. Zawar V, Kirloskar M, Chuh A. Fixed drug eruption - a sexually inducible reaction?. Int J STD AIDS. 2004 Aug. 15(8):560-3. [View Abstract]
  62. Tornero P, De Barrio M, Baeza ML, Herrero T. Cross-reactivity among p-amino group compounds in sulfonamide fixed drug eruption: diagnostic value of patch testing. Contact Dermatitis. 2004 Aug. 51(2):57-62. [View Abstract]

Targetoid fixed drug eruption on the abdomen of a child.

Hyperpigmented fixed drug eruption on the hip of an adult.

Vesicular fixed drug eruption on the glans penis.

Multiple hyperpigmented fixed drug eruptions on the trunk.

Hyperpigmented fixed drug eruption on the right side of the upper lip.

Acute interface dermatitis with prominent vacuolar change and individual necrotic keratinocytes within the epidermis (X10).

Interface dermatitis, vacuolar change, necrotic keratinocytes, and incontinent pigment in the dermis (X40).

Targetoid fixed drug eruption on the abdomen of a child.

Hyperpigmented fixed drug eruption on the hip of an adult.

Vesicular fixed drug eruption on the glans penis.

Multiple hyperpigmented fixed drug eruptions on the trunk.

Hyperpigmented fixed drug eruption on the right side of the upper lip.

Acute interface dermatitis with prominent vacuolar change and individual necrotic keratinocytes within the epidermis (X10).

Interface dermatitis, vacuolar change, necrotic keratinocytes, and incontinent pigment in the dermis (X40).

AcetaminophenAcyclovirAllopurinolAllylisopropyl-acetylureaAmide local anesthetics
AtenololBarbituratesBotulinum toxinCarbamazepineCashew nut
CeftriaxoneCelecoxibCetirizineChloral hydrateChlordiazepoxide
ChlorhexidineChlormezanoneChlorphenesin carbonateCiticolineClarithromycin
Cyproterone acetateDextromethorphanDimenhydrinateDiphenhydramineDipyrone
DocetaxelEperisone hydrochlorideErythromycinEthenzamideFeprazone
Iodinated radiography contrast mediaIomeprolKakkonKetoconazoleLactose


LormetazepamMagnesium trisilicateMefenamic acidMelatoninMethaqualone
NaproxenNimesulideOmeprazoleOndansetronOpium alkaloids
OxyphenbutazonePaclitaxelPamabromPapaverinePara-aminosalicylic acid
PhenylpropanolaminePhenytoinPipemidic acidPiroxicamProcarbazine
Sodium benzoateStrawberriesSulfamethoxazoleTartrazineTerbinafine
Tolfenamic acidTosufloxacinTranexamic acidTrimethoprimTropisetron