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Acneiform Eruptions Clinical Presentation

  • Author: Julianne H Kuflik, MD; Chief Editor: Dirk M Elston, MD  more...
 
Updated: Feb 08, 2016
 

History

Patients with acneiform eruptions present with acnelike lesions such as papulonodules, pustules, and cysts. They typically do not present with comedones, which is a distinguishing factor. The physical location may be outside of the area in which acne vulgaris occurs. Acneiform eruptions can be distinguished from acne vulgaris by a history of sudden onset, monotonous lesion morphology, and development of the eruption at an age outside the range typical of acne vulgaris. In the case of drug-induced acneiform eruptions, the eruption resolves with discontinuation of the medication.

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Physical

Nevus comedonicus (NC) is an infrequent developmental anomaly manifesting as aggregated open comedones. It consists of dilated follicular or eccrine orifices plugged with keratin. Also known as comedone nevus and nevus acneiformis unilateralis, it may be solitary, congenital, or, less frequently, can occur later in life as a result of occupational exposure. The differential diagnosis of NC includes familial dyskeratotic comedones and linear comedone formations usually linked with acne vulgaris or chronically sun-damaged skin (Favre-Racouchot disease). Infrequently, multiple comedones in other unusual contexts may raise NC as a possible consideration. Treatment of NC is generally surgical, through excision or carbon dioxide laser ablation of the involved skin. Medical therapy with topical retinoids may be of some benefit. For more information, see Nevus Comedonicus.

The eruptive vellus hair cysts[6] manifest as flesh-colored papules found usually on the face, chest, neck, thighs, groin, buttocks, and axillae. They represent an anomaly of the vellus hair follicles and may be hereditary. Histopathology reveals a mid dermal epithelial cyst containing vellus hairs and keratinous material. These cysts may undergo spontaneous regression, form a connection to the epidermis, or undergo degradation with a resultant foreign body granulomatous formation. Treatment is often difficult. Incision and drainage of individual lesions carries the risk of subsequent scarring, and modalities such as carbon dioxide laser ablation are difficult to use over large surface areas. Topical retinoids and 12% lactic acid preparations have proven useful in some instances. For more information, see Eruptive Vellus Hair Cysts.

Steroid acne[7, 8] is observed as monomorphous papulopustules located predominantly on the trunk and extremities, with less involvement of the face. Characteristically, it appears after the administration of systemic corticosteroids, including intravenous therapy. Topical or inhaled corticosteroids may cause an acneiform eruption of the area of skin under which the topical preparation is applied or in around the nose or mouth in the case of inhaled steroids. The eruption usually resolves after discontinuation of the steroid and, in addition, may respond to the usual treatments of acne vulgaris. For more information, see Acne Vulgaris.

Exposure to halogenated aromatic hydrocarbon compounds, such as chlorinated dioxins and dibenzofurans, by inhalation, ingestion, or direct contact of contaminated compounds or foods induces a cutaneous eruption of polymorphous comedones and cysts referred to as chloracne. Other associated skin findings may include xerosis and pigmentary changes. Internal changes involving the ophthalmic, nervous, and hepatic systems may also occur, and some chloracnegens can be oncogenic. Treatment is difficult because chloracne may persist for years, even without further exposure. Chemicals that contain iodides, bromides, and other halogens can also induce an acneiform eruption similar to that of steroid acne; however, the iodide-induced eruption may be more extreme.

Antibiotics may induce an acute generalized pustular eruption. Penicillins and macrolides are the greatest offenders. Patients usually are febrile with leukocytosis, and the eruption does not usually involve comedones. Other implicated antibiotics include co-trimoxazole, doxycycline, ofloxacin, and chloramphenicol. Other types of medications can also produce an acnelike eruption, including corticotropin, nystatin, isoniazid, itraconazole, hydroxychloroquine, naproxen, mercury, amineptine,[9, 10, 11] the antipsychotics olanzapine and lithium, chemotherapy drugs, and epidermal growth factor receptor inhibitors.[12, 13, 14, 15, 16, 17, 18, 19] For more information, see Drug Eruptions.

Various infections may also display an acneiform pattern. Gram-negative folliculitis, a persistent papulopustular eruption, may be a complication in patients on prolonged treatment with oral antibiotics for acne vulgaris or rosacea. Antibiotic use, such as those of the tetracycline class, can alter the normal skin flora of the skin allowing for growth of gram-negative organisms in the nares of the nose. These gram-negative organisms are typically spread to the skin of the upper lip, chin, and jawline whether they cause a folliculitis. Culture of the papulopustules grows gram-negative bacilli and gram-negative rods, including Escherichia coli and Klebsiella, Enterobacter, and Proteus species. Typical history is a patient with a sudden acne flare despite no change in treatment or a patient unresponsive to traditional therapies. Oral isotretinoin is considered standard of care. For more information, see Gram-Negative Folliculitis, Acne Vulgaris, and/or Rosacea.

Pityrosporum folliculitis is another infectious folliculitis that is presumably caused by a host reaction to the yeast Malassezia furfur, previously named Pityrosporum ovale, a normal human skin commensal organism. It appears primarily on the trunk and upper extremities of late adolescents and young adults. Unlike acne vulgaris, it is pruritic, does not contain comedones, and responds to empiric antifungal therapy rather than antibiotics. Diagnosis is typically made clinically, although the yeast and hyphae can be observed in biopsy specimens in the widened follicular ostia along with keratinous material, and occasionally, rupture of the follicular wall may occur. Patients may be treated with topical leave-on, wash-off, or systemic antifungal therapy. For more information, see Pityrosporum Folliculitis.

Eosinophilic pustular folliculitis (EPF) is a disease of unclear etiology, thought to be an allergic hypersensitivity. It appears as a recurrent pruritic papulopustular eruption on the face, trunk, and extremities. Histopathology reveals a predominantly perifollicular infiltration of eosinophils with some mononuclear cells and subcorneal pustules composed of eosinophils. Three main types exist, (1) infantile form, (2) HIV associated, and (3) classic Ofuji disease in immunocompetent patients, typically Japanese patients. Patients may also demonstrate blood eosinophilia and leukocytosis. Treatment modalities and results vary greatly. Options include topical and systemic corticosteroids, oral antibiotics, dapsone, isotretinoin, and pulsed ultraviolet phototherapy (PUVA). Indomethacin is the treatment of choice for classic Ofuji disease. For more information, see Eosinophilic Pustular Folliculitis.

Several infectious diseases may result in acneiform eruptions, as follows:

  • In secondary syphilis, papulopustules and nodules, some crusted, may occur on the face, trunk, and extremities. The causative agent, the spirochete Treponema pallidum, may be easily observed in biopsy specimens with the Warthin-Starry stain. In addition, serologic tests and the presence of spirochetes on darkfield microscopy may reveal the diagnosis. For more information, see Syphilis.
  • Mycotic infections may also manifest cutaneously with papules and nodules that may ulcerate and crust.
  • Sporothrix schenckii, the responsible agent of sporotrichosis, commonly induces a lymphocutaneous reaction, but it can also produce a persistent fixed localized cutaneous papulonodular eruption that may involve the face. The organism can be demonstrated histologically, by peripheral blood smear, and by fungal culture. For more information, see Sporotrichosis.
  • Cutaneous coccidioidomycosis usually caused by inhalation and dissemination of Coccidioides immitis, may rarely occur by primary inoculation and appear as papulopustules, nodules, or plaques that can eventually ulcerate and crust. For more information, see Coccidioidomycosis.

Rosacea appears similarly to acne vulgaris with papulopustules on the face, but in addition, patients may also have facial flushing and telangiectasias. Patients with rosacea, however, lack comedones. Four subtypes of rosacea exist: (1) erythematotelangiectatic, (2) papulopustular, (3) phymatous, and (4) ocular.

Rosacea is more common in the white population and in women in the third and fourth decades of life. Men, however, more commonly develop sebaceous hyperplasia of the nose, known as rhinophyma. Associated eye findings are variable but include blepharitis, conjunctivitis, iritis, iridocyclitis, hypopyon iritis, and even keratitis. Although the definitive etiology is unknown, weather extremes, hot or spicy foods, alcohol, and Demodex folliculorum mites can trigger and exacerbate this condition. Acne rosacea has also been associated with the ingestion of a high-dose vitamin B6 supplement.[20]

Histopathology of rosacea skin reveals granulomatous inflammation. Treatment primarily includes skin barrier sunscreens and topical antibiotics such as metronidazole, retinoids, and oral tetracyclines.

Perioral dermatitis, also a disorder of unclear etiology, is mainly observed in the young, white, female population as papulopustules with erythematous base. The eruption is predominantly perioral in location, characteristically sparing the vermilion border of the lip, but it may also include the perinasal and periorbital areas. A variant known as periocular dermatitis affects the skin around the eyes. The eruption is thought to be a variant of rosacea, as biopsies show changes similar to those of rosacea.

Causative agents are theorized to be prior use of topical corticosteroids, but neither duration of use nor steroid strength have been shown to be clearly related. Demodex mites,[21] moisturizers, fluorinatced compounds, and contact irritants or allergens have also been implicated as causes of eruption.

Therapy typically includes cessation of topical steroids or other offending agents and topical anti-inflammatory treatments such as topical metronidazole, topical pimecrolimus cream, azelaic acid, as well as oral anti-inflammatory dose antibiotics such as doxycycline. For more information, see Perioral Dermatitis.

Lymphoma has been reported as a cause of acneiform eruptions.[22]

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Causes

See Physical.

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Contributor Information and Disclosures
Author

Julianne H Kuflik, MD Assistant Clinical Professor of Dermatology, Department of Dermatology, Rutgers New Jersey Medical School

Julianne H Kuflik, MD is a member of the following medical societies: American Academy of Dermatology

Disclosure: Nothing to disclose.

Coauthor(s)

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.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Jeffrey Meffert, MD Associate Clinical Professor of Dermatology, University of Texas School of Medicine at San Antonio

Jeffrey Meffert, MD is a member of the following medical societies: American Academy of Dermatology, American Medical Association, Association of Military Dermatologists, Texas Dermatological Society

Disclosure: Nothing to disclose.

Chief Editor

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

Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology

Disclosure: Nothing to disclose.

Additional Contributors

Joshua A Zeichner, MD Assistant Professor, Director of Cosmetic and Clinical Research, Mount Sinai School of Medicine; Chief of Dermatology, Institute for Family Health at North General

Joshua A Zeichner, MD is a member of the following medical societies: American Academy of Dermatology, National Psoriasis Foundation

Disclosure: Received consulting fee from Valeant for consulting; Received grant/research funds from Medicis for other; Received consulting fee from Galderma for consulting; Received consulting fee from Promius for consulting; Received consulting fee from Pharmaderm for consulting; Received consulting fee from Onset for consulting.

References
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