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THERAPY IN PRACTICE Folliculitis Recognition and Management Jestis Luelmo-Aguilar and Mireia Sabat Santandrew Unity of Dermatology, Hospital of Sabadell, Sabadell, Spain Contents Abstract 1. Clinical Evaluation 2. Laboratory investigation 3. Clinical Presentation and Management 3.1 Infectious Fosiculis 3.1.1 Bacterial Folicultis 3.12. Syphilic Folicults 3.13. Fungal Folicuitis 3.14 Virol Folicults 3.15. Parostic Folleultis 32 Nonntectious Folicults 3.2.1 Follcultis of Known Etiology 322 Follcultis of Uncertain Biology 3.23 Follcultis Associoted with HIV Infection 3.2.4. Skin Disorders with Folicular Expression 33 Psoudofolicults 4. Conclusions SSSSRRSSSeeesesss Abstract Follicults is an inflammatory reaction in the superficial aspect of the hair follicle and ean involve the follicular opening or the perifollicular hair follicles, The pilosebaceous unit of the follicle is divided imo three ‘compartments: the infundibulum (superficial part, outlined by the sebaceous duet), the isthmus (between the sebaceous duct and arrector pili protuberance), and the inferior segment (stem and hair bulb). This anatomical scheme forms the basis for any evaluation of the cline: estations of folliculitis. Most of the follicular conditions can be classified according to their anatomical location and histopathologic patterns. Clinically. the inflammation manifests as Imm-wide vesicles, pustules, or papulopustules in acute cases; however, hyperkera- tosis and keratotie plug formations are indicative of a chronic process. The presence of superficial pustules does not always imply an infectious origin, as there are many noninfectious types of folliculitis. In this review, we describe the different types of folliculitis basod on their etiology, clinical manifestation, and treatment, We also discuss some newly described disorders and the latest information on their treatment Follicuitis is an inflammatory reaction inthe supe aspect basis for any evaluation of the clinical manifestations of follicu- of the hair follicle and can involve the follicular opening or the perifollicular hair follicles. The piloscbaceous unit ofthe follicle is divided into three compartments: the infundibulum (superficial part, outlined by the sebaceous duct), the isthmus (between the sebaceous duct and arrector pili protuberance), and the inferior (stem and hair bulb). This anatomical scheme forms the Ins, 1. Clinical Evaluation Clinical information is very useful in recognizing the causes of folliculitis, Pruritus is the most frequent symptom, as is common in other inflammatory skin dermatoses. A detailed history is needed to determine the etiology." Itis very important to question Lacino- Aguilar & Sabet Santandren 02 es No ‘Swab othe lesions Ask about Por kb Seroiogy HN rug intake Seroiogy hepa vrs specu heated water Serology syphilis Contiminfction Hisiopathologie sty corraatonshe Cont floats Fig, 1. Agoritum for the clinical evaluation of flicults. PCR = polymerase ‘chain reaction the patient about predisposing factors 10 cutaneous infections, including: drug abuse; an underlying immune deticiency; expo- sure to possibly contaminated heated water (hot tub, spa bath, heated swimming pool, or bath water); and exposure to kittens, guinea pigs, or farms. Its also important to know the patient's age, sex, race, job, and the possibility of other associated dermati- tis. A physical examination usually shows the highly characteristic ‘elementary lesions formed by follicular and perifollicular pustules, papules, and papulopustules, but in some cases there is a predo nance of papules or keratotie plugs. Noting the location and distribution ofthe lesions is very helpful, as is knowledge of their ‘evolution, An algorithm for the linical evaluation of folliculitis is given in figure 1 2, Laboratory Investigation Swabs and Gram stains of the pustule content should be rou- Linely collected 0 exclude a diagnosis of bacterial oF viral follicu- litis. Scrapings should also be taken for fungal culture. A potassi- um hydroxide preparation may identify a yeast form or candida. In addition, a Tzanck smear is useful in cases of herpetic. viral folliculitis. If 2 predisposing fa serological tests for HIV or syphilis viral folliculitis, the diagnosis can be confirmed by polymerase cchain reaction (PCR). Histopathologic studies enable a correct classification and diagnosis if the patient so requires. 3. Clinical Presentation and Management 3.1 Infectious Folicullis 3.1.1 Bactertal Folicultis Bacterial folliculitis may be superfieial or deep. Superficial folliculitis (Bockhart impetigo) consists of small pustules, often surrounded by aring of erythema located within follicular orifices ‘The pustules develop in clusters and form crusts during the evolu- ‘9 om Dateien BY Agr ates tion of the folliculitis, often involving the face, buttocks, and axilla in infants and children: the legs in adolescent girls; and the flexural areas in adolescent boys. The pustules usually heal im a few days but occasionally develop into furuncles. Bacterial folliculitis usually occurs in children or adults with a predisposing factor that helps to increase the number of bacteria on the surface ofthe skin (able 1). Staphylocaccus aureus is the most frequent causative agent, and species of Sireprocoeens, Prete domonas, Proteus, and coliform bacteria have also been implical- cd in the infection." Pseudomonal folliculitis involves the ex- posed aspects othe trunk and follows an exposure to contamina- ted water (figure 2) Furuncles occur as a result of the spread of bacterial infection Wo the tissues of the follicle, beneath the infundibulum, either at the onset of infection or during the evolution of superficial follicu- Titus. A furuncle begins asa small, painful follicular inflammatory nodule that becomes pustular and in few days develops central necrosis, and heals after a discharge of necrotic material, leaving a permanent scar (figure 3). Staphylococei are the most common ausative organism, including S. epidermidis, and strepioco coliform bacteria have also implicated in some cases. Furuncles are more common in young adults, especially boys, and the most affected areas are the face, back of the neck, breasts, axillae, Perincum, buttocks, and thighs. Predisposing factors for the devel- ‘opment of furunculosis include: chronic staphylococ diabetes meltitus, malnutrition, and HIV infection, Bacterial sycosis is a subacute or chronic staphylococcal inlee- tion that involves the entire hair follicle. The condition occurs in males after puberty, most frequently in the third and fourth de- cades of life. The lesions begin with an edematous, inflammatory follicular papule or pustule located in the beard (usually on the upper lip), accompanied by @ burning sensation. In a few days numerous pustules develop, involving the neighboring follicles, that may coalesce to produce plaques studded with pustules. The 1ay persist for Years and in Some severe cases are destroyed by searring.™"! cchronie form (lupoid sycosis) the folli Table |. Factors predisposing bacterial folicuitis ‘Nasal earage of Staphylococcus aureus cctusion Maceration Hypernydration Complicating pruic skin diseases (2.9, scabies, eczemas) ‘Vigorous application of topical medications (corticosteroids) ‘Shaving against the erection of hale growth (olicultis on leg) Exposure to ails and certain chemicals Pin worm infestation (olicults of buttocks) Exposure to heated water (hot tub, heated swimming poo!) or contaminated wat Amn Dermat 28 55) Recognition and Management of Folhlitis 305, Fig, 2. Pseudomonas fliculis: infammatory pruriginous papulopustulous rash, localized on the chest. Superficial bacterial folliculitis usually responds to treatment with topical antibacterials such as mupirocin or fusidie acid oint- ment, Gram negative folliculitis needs to be identified and elimi- c ofthe infection. Although superficial bacter- ial folliculitis often resolves spontaneously, some patients require oral antibacterial treatment, such as ciprofloxacin (table II). nated from the sou To eradicate skin color ation in Bockhart impetigo (superfi- cial folliculitis) caused by staphylococeal infection the patient should be advised to take a S-minute daily bath with Oilatum® ' liquid paraffin compound with moisturizing and antiseptic proper tics, plus bath oil in the bath water for a minimum of 4 weeks. In addition, to eradicate clothing contamination, clothing, linen, and towels should be routinely washed in hot water. Finally, predis- posing factors need to be identified and eliminated. In cases of deep bacterial folliculitis, an appropriate oral anti~ bacterial, based on the results of the culture, is mandatory ! Incision and drainage may sometimes also be necessary 3.1.2 Syphitc Folicuitis Secondary syphilis is charaeterized by various types of eutane~ fous lesions. Pustulous syphilis is infrequent and the lesions may present as a pustulous, papulo-pustulous, or papule-crust rash without fever. Acneiform syphilis is a form of granulomatous perifolliculitis in late syphilis with circinate papular-nodular te- sions. The diagnosis of this infection requires an accurate history and strong clinical suspicions!" 3.1.3 Fungal Follicults Superficial mycoses are very common, They are divided into three groups: dermatophytic, pityrosporum, and candida follicu- Dermatophyic Flicutts Dermatophytic folliculitis is usually caused by a zoophilic species and can produce different types of clinical manifestation according to the infected body area, including: tinea capitis, tinea barbae, tinea corporis, tinea cruris, and tinea pedis." This condi- tion presents clinically as follicular pustules surmounting an indu- rated erythematous plaque with peripheral extension, Hair shalt loss is typical and depends on the degree of inflammation, which relates to the depth of penetration ‘The most important form of dermatophytic folliculitis is tinea capitis, which mainly affects children and has four variants: (i) noninflammatory; (i) “black dov’; (ii) favus; and (iv) kerion. ‘The first two forms are usually nonscarring with minimal inflamma- tion, whereas the later two involve severe suppurative and granu- lomatous folliculitis and permanent hair loss. ‘When treating tinea capitis, topical antifungals are not effec- tive, Nevertheless, to decrease sporax spread, an antifungal sham- poo can be used (table I). In children, griseofulvin (10-20 mgrke day) for a minimum of 6 weeks remains one of the first steps in ‘eatment, Good results have been achieved with terbinafine (125 mg/day, 6 weeks). ‘Trichophytie granuloma (Majocchi granuloma) is a classical type of inflammatory tinea corporis located on the legs with perifollicular granulomatous papules, primarily caused by Trichophyton rubrum?” Tinea barbac is a disease that mainly affects adult males, usually in the beard and moustache areas, Infections caused by zoophilic species are responsible for the great majority of cases; the two main species involved are T. mentagrophytes and T. verrucosum. Clinically. tinea barbae displays deep folliculitis with red inflammatory papules and pustules and exudation or rusting. ‘Hair shaft loss is also present (figure 4). Kerion and favus are both deep suppurative types of folliculitis infecting the scalp, which are usually complicated by pain, fever, Fig. 9. Recurrent furunculosis in an immunosuppressed woman. 1 The use of trade names is for product identification purposes only and does aot imply endorsement ‘9 om Dateien BY Agr ates Amn Dermat 28 55) sos 1 Sabot Santandron Lacino- Agus Table I, Treatmont of infectious folliculitis Type of foticitis Topical ‘Systeme Staphylococcal Fusicie acd or mupirocin Dicloxaciin, fucioxaciin, land streptococcal ointment (td) tusoic aid, athromycln Gram-negative Dilute acid acetic baths Ciprofloxacin bacteria (pseusomonas)* Dermatophytes Antifungal shampco _—_Griseofulvn, terbinafine, lraconezole Piiyrosporum Topical azoles, shampoos with sulur of selenium candidal Itraconazole Horpatic Aciclovir, valaciclovir, anthistamines Molluscum (pox Curettago, cryotherapy, ius) canthariin, ppodophylotoxin, trichloroacetic acid Demodicidosis 5% permethrin cream Itraconazole, ivermectin ‘Usually resolves spontaneously. tl = thee time and regional lymphadenopathy that results in scarring and perma nent hair loss. Kerion is caused predominantly by Microsporum canis and T. verrucosum, and favus, the more severe form, is caused by T: schoenleinit (figure 5), In these eases oral therapy is essential (griseofulvin, terbina- fine), Piyrosporum Folicultis Pityrosporum folliculitis is caused by pityrosporum yeasts, most commonly Pityrosporum orbiculare. The condition mainly affects teenagers and men, probably as a result ofthe production of free fatty acids by the yeast and blockage of the follicular ostium by scale." The lesions are erythematous follicular papules and pustules located on the back, upper trunk, and shoulders, and are frequently pruritic. Treatment with a topical antifungal is usually effective (lable 1D." Cone albicans Pustular folliculitis caused by Candida albicans is a rare condi- tion reported in individuals who abuse heroin; the condition in- volves candidemia, leading to pustules and nodules in the hair- bearing areas, Pustular folliculitis has also been reported in healthy individuals, with widely distributed and painful pustules." Candidal folliculitis must be treated with oral itraconazole (200 mg/day), ‘9 om Dateien BY Agr ates 3.1.4 Viral Foticuts Folliculitis due to herpes simplex virus (HSV) and molluscum contagiosum is a rare condition and might be considered a sign of | lly in cases caused by molluscum contagiosum,""*") The clinical presentation in HSV-induced fol- immunosuppression, especi liculitis involves. prurt papulovesicles with crusts or umbili Molluscum contagiosum folliculitis presents as multiple discrete pruritic whitish papules over the beard area. Frequently, patients with herpetic folliculitis have a history of recurrent herpes infec- tions on the face. Further investigation is mandatory, especially in ceases of molluscum contagiosum folliculitis that occurs in immu- nocompetent subjects, or that may be a sign of underlying immune deficiency, such as HI Of folliculitis caused by herpes zoster infection." ‘multiple erythematous. papules or ed vesicles on the face fection. There are several some reports In viral herpetic folliculitis, the recommended treatment is oral antihistamines or aciclovir 200mg five times daily for $ days." ‘There are different modalities to treat molluscum contagiosum folliculitis, the most common is cutterage (table I). 3.1.5 Parasitic Follcultis Demodex spp. mites normally inhabit the hair follicles and sebaceous glands. Only D. folliculorum and D. brevis are found in humans, both in sebaceous areas such as the chest, back, temple, periorbital area, and nose. D. folliculorum has been implicated in many dermatitides characterized by the presence of numerous mites, such as rosacea-like eruptions on the face, perioral dermati- tis, pityriasis folliculorum, blepharitis, eosinophilic pustular fol- Ticulitis, and papular lesions associated with AIDS (figure 6). ‘Typically, all of these dermatoses respond rapidly to appropriate therapy with 5% permethrin cream (topical) or ivermectin (systemic). (7) raconazole or Fig. 4. Tinea barbae: typical location on the moustache, with hairloss and high inflammatory response. Amn Dermat 28 55) int of Follicaitis Recognition and Manag 05 Fig. 5. Favus: crust, exudation, and pustulation with hairloss on a young boy's head, 3.2 NorInfectious Folicultis 3.2.1 Foliculfs of Known Etiology Acnaiform Folicuits Acneiform folliculitis is frequently drug induced. The use of systemic and topical corticosteroids and corticotropin can result in follicular skin eruptions consisting of small and inflammatory pustules distributed over the face, chest, shoulders, neck and upper back. Lithium typically produces an acneiform eruption and fol- liculitis in the same areas as aene vulgaris, or it may be more extensive; the condition begins within days of starting Tithium treatment, may be pruritic, and resolves quickly with discontinua- tion, Halogens such as bromides and iodides that are administered systemically may produce an aeneiform eruption similar to corti- costeroid-induced acne but more extensive and. inflammatory. ‘Tuberculostatic drugs such as isoniazid and rifampin (rifampicin) ‘can produce acneiform eruptions."2 Occupational acne appears after exposure to cutting il, dichlorodiphenyltrichloroethane (DDT), halogenated. hydro bons, crude coal tars, asbestos, and heavy destilated water, The ccruption consists of inflammatory pustules, papules, comedone and nodules, located on covered areas such as the buttocks, thighs, and forearms. Exposure to chlorinated aromatic hydrocarbons, produces an acneiform skin reaction called chloracne, character= ized by open and closed comedones with many inflammatory cysts located on the face (malar eminences, temples, postauricular areas, and neck), In cases of folliculitis with known etiology, the treatment is obvious: avoid the cause and correct the possible deficiencies Anti-acne topical therapies are sometimes needed. Some neiform dermatoses, especially those induced by drugs, respond well to topical tretinoin (vitamin A acid) treatment.) ‘9 om Dateien BY Agr ates Folicultis Caused by Nutitiona! Deficiencies Severe vitamin C deficiency causes scurvy. It requires about 2 ‘months of deprivation to produce mucocutaneous signs, including: perifollicular petechiae, follicular hyperkeratosis, gingival hemor- shage, and hyperplasia. The follicular eruption occurs on the lowers legs, anterior forearms, and abdomen = One of the earliest signs of vitamin A det blindness. The skin shows follicular hyperker generalized wrinkling." xy is night osis, dryness, and Actinic Superficial Folicultis Ac both sexes. It always occurs within 2448 hours of sun exposure and is characterized by numerous sterile follicular pustules on the shoulders, trunk, and arms, accompanied by a burning sensation, It usually resolves within 10 days, Sunsereens provide partial protec- tion 3) ie folliculitis was deseribed in 1985 in young adults of 3.22 Folliculis of Uncertain Etiology ‘Acne Wugors ‘Acne is one of the most prevalent dermatoses in adolescents, ‘and involves the face and upper trunk. The origin of the acne lesions is an alteration, with or without inflammation, in the follicular apparatus that forms comedones, papules, pustules, nod- ules, or cysts. ‘Acne vulgaris has many different modalities of treatment ‘Topical antibacterial treatment is now recommended less than it used! to be, and only for short periods, to avoid the development of resistances. ‘The combination of topical retinoids, particularly adapalene (a retinoid-tike agent), with topical antibacterials or azelaic acid is one of the most efficacious therapies. Oral therapy options include different antibacterials. (minocycline, doxyeyeline), isotretinoin, and oral contraceptives!™! Fig. 6. Dermodex folicultis: excorated papules on the face of a child with atopic dermatitis, Amn Dermat 28 55) 306 Lacino- Aguilar & Sabet Santandren Table Il Treatment of follcultis of uncertain etclogy ‘Type of foicutis Topical Systemic Comment ‘Acne keloldalis Potent coricosteroid ‘Oral antibacterial (etacycine) Th combination; fang term (fuocinonida) Folicullts dacalvans Mupitocin Fifampin (ifarpicin) + clindamycin, — In combination; long term {use acd, tyrosine (L-yrosine), zine Metronidazole, minocycine, oxyeyciine, clarithromycin, isotretinoin Rosacea 1% metronidazole, 20% azelaic ‘acd cream, retineid Peroral dermatitis Fox-Fordyco disease Iciopathic folicular mucinosis Perforating folicults Disseminate and recurrent Infundibuototicults Eosinophilic pustular folicultis 19% metronidazole Clindamycin solution Corticosteroid, tacrolimus Tetracycine, erythromycin ral ratinoids, surgory Phototherapy, minocycline ‘Alopurino| Isotretincin Naproxen, cattizine, corticosteroid Eradicate Helicobacter pylort or ‘Demedex foliculorum infection; tacrolimus for corcosteroid-induoed Discontinue topical corticosteroid Usually selttiited Spontansous resolution Keloidal Folicults (Acne Keloldalis Nuchoe) Keloidal folliculitis or acne keloidalis nuchae is a chronic, scatring folliculitis that mostly affects Black patients, The lesions. are located on the back of the neck and the occipital sealp. Itbegins as small, firm papules and oceasional pustules that progress 10 eloidal papules and plaques and progressively lead to hyper- twophic scars, chronic abscesses, and hair loss. The cause remains unknown and can be multifactorial") Keloidal folliculitis has been associated with sebortheic dermatitis, acne vulgaris, and tufted hair folliculitis.) At present there is no appropriate therapy for acne keloidalis ‘Some authors recommend a combination of a potent topical co costeroid with prolonged use of an oral antibacterial, such as tetracycline (table HD." Treatment of folliculitis decalvans is also very difficult. There are reports demonstrating @ good res- ponse to oral fusidic acid and zinc treatment.!"! Anecdotal reports suggest that shaving the sealp may be a successful strategy. The best treatment seems to be an early course of rifampin combined with clindamycin. ICs not advisable to use rifampin alone, due to the rapid emergence of stapinylococcal resistance. Folicultis Decavans Folliculitis deealvans is characterized clinically by chronic folliculitis that leads to progressive scarring and alopecia, It may involve the scalp alone or together with any other hairy regions. It initially presents as crops of follicular pustules, followed by de- struction of the hair shaft and slow progression of the alopecia Some recent reports suggest the possibility of a genetie predisposi- on.21§, qureus infections seem to play an important role in the pathogenesis of this anomaly.) ‘9 om Dateien BY Agr ates Rosacea Rosacea is a common condition of unknown etiology. Many possible causes have been described such as genetic predisposi- tion, Helicobacter pylori infection, and D. folliculorwm infestation ‘among others, It occurs in middle-aged men and women as a result of an inflammation within and around follicular infundibula. The lesions consist of papules, pustules, and telangiectasia that affect the face and nose, Most cases of rosacea respond well to long-term topical anti- bacterial treatment, such as 1% metronidazole or 20% uzelaie acid cream (table ID. Oral or topical retinoids may also be effective Systemic treatment options for rosacea include metronidazole, minocycline, doxycycline, clarithromycin, and isotretinoin! Many authors recommend the eradication treatment of H. pylo- ris! while others recommend 10% erotamiton, 5% permethrin, and oral or topical ivermectin 10 treat D. folliculorum infec tion"! Tacrolimus can be useful in corticosteroid-induced a0) rosacea, Petioral Dermatitis Perioral dermatitis is most frequent in childhood and in young women. Its exact origin is not known, Skin lesions consist of flesh- colored or inflamed papules, micronodules, and pustules with variable pruritus. The condition is probably a localized form of rosacea with the same clinical lesions but restricted to the perioral region and lower eyelids. The only clearly associated factor with this condition is the use of Muorinated topical corticosteroids. Greasy cosmetics and hyperandrogenemia are also implicated in the etiology of perioral dermatitis. ‘Treatment of perioral dermatitis consists of discontinuing topi- cal fluorinated corticosteroid use, if any, and using topical metro- Amn Dermat 28 55) int of Follicaitis Recognition and Manag 307 nidazole alone or in combination with either oral tetracycline or erythromycin (table HID! Successful treatment with topical adapalene has also been reported recently. ForFordyce Disease: Fox-Fordyce disease is a chronic condition involving itehy, rounded, follicular papules localized to the areas of the skin containing apocrine sweat glands, such as axillae, pubes, areolae, and periumbilical and presternal areas, This distribution of skin changes suggests an apocrine origin, affecting the follicular infun- dibulum ar the site of entry of the apocrine duct. I is nine times ‘more frequent in women than men and occurs between the ages of 13 and 35 years. 1e has been successfully treated with a topi- solution, with oral retinoids, and with surgery Pruitie Folicultis of Pregnancy Prutitic folliculitis of pregnancy (PEP) was first described in 1981.0 PEP is a generalized pruritic, erythematous, papular ‘eruption occurring in pregnant women, Some authors suggest that PEP should be included under the polymorphie eruption of preg- nancy.) Pathologic features of the condition correspond to sterile folliculitis, but the etiology is unknown, No morbidity to the ‘mother of fetus has been observed, and the eruption was found to clear spontaneously in the postpartum period!" Eosinophilic Pustula Folicuitis Eosinophilic pustular folliculitis (EPF) was first described by Ofuji ct al. in 1970 in three Japanese patients. However, the etiology is uncertain. There are three different variants: classic EPF or Ofuji disease; BPF associated with HIV infection; and the infantile form of EPP. ‘The classic form is characterized by recurrent outbreaks of follicular erythematous papules and pustules that may coalesce to orm polyeyelie plaques, with central healing and peripheral ex- tension, It is often pruritic and usually involves seborrheic distr- bution, but may also be found in 20% of patients on the trunk, proximal extremities, palms, and soles of the feet. EP associated with HIV infection is often different from the classic form and may include erythematous non-follicular papules, urticariform lesions, large erythematous plaques, or even a genera- lized rash, The face, runk, and extremities can be affected, but not the palms and soles (figure 7). This variant is usually chronic and persistent. Its always very pruriginous and often heavily excoriat- ed 9551 Infantile EPF presents as numerous sterile pustules located on >90% on the scalp, although it can also affect the trunk, face, and ‘extremities. It usually begins in the neonatal period 56°) The histologic image of EPP, with the pilosebaceous structure infiltrated by # mixture of eosinophils and neutrophils, is not seen in any other entity.0%! ‘9 om Dateien BY Agr ates Eosinophilic pustular folliculitis has many treatments, inelud- ing naproxen, topical and oral corticosteroids, and cetirizine (table MID.557 Some recent cases not associated with HIV infection hhave been reported; these were treated with tacrolimus ointment with good results Spontaneous resolution can oecur. In eases of EPF associated with HIV infection, as with most of the other HIV- associated dermatoses, the best treatment seems to be combination therapy and the restoration immunity.!655) Toxic Erythema of the Newbomn Toxie rythema of limiting pustular eruption of the neonatal period of unknown etiology. The rash is composed of erythematous macules, papules, pustules, or a combination of these elements, Lesions may occur anywhere and appear during the first 3-4 days of life and fade during the following 2 week period. No therapy is indicated '*4#1 newborn represents a benign, sell Follicular Muclness Follicular mucinosis or alopecia mucinosa is an inflammatory disorder characterized clinically by follicular papules and more o less indurate plaques. The face and neck are_most commonly involved. It can be classified into two groups. The first type is the most common and benign form; in younger patients it is often limited to a few lesions on the head and neck, whereas in older patients it often involves more lesions in a more generalized distribution, Lesior second type, which presents in elderly patie plaques, coexists with a malignant lymphoma, especially mycosis fungoides.) spontaneously resolve within 2 years. The as disseminated ‘The idiopathic form of follicular mucinosis has been treated with phototherapy and minocycline (lable IID. In addition, there are some cases of acquired reactive perforating dermatoses successfully treated with allopurinol Fig. 7. Eosinophilic pustulous follcults in an HIV-niected man with ery- thematous, inflammatory papules, and some urticarial lesions, Amn Dermat 28 55) sos Lacino- Aguilar & Sabet Santandren Perforating Folicultis Included among the perforating disorders, perforating follieu- isis more frequent in women and may persist for many years. It presents as an asymptomatic eruption of small follicular keratotic papules on the buttocks and the extensor surfaces of the ext lies, There is a relationship with diabetic nephropathy." Disseminated and Recurrent infundibuiotolicults Disseminated infundibulofolliculiti is an uncommon condition that occurs mainly in Black patients. Clinically it presents as multiple disseminated follicular pinpoint papules on the trunk and limbs, sparing the flexures. Pruritus is often present and the ‘course ischronic or recurrent and usually unresponsive to local or systemic treatment; however, some cases will respond to isotre- tinoin therapy £71 Disseminated and recurrent infundibulofolliculits is often self mited and usually unresponsive to treatment. Occasional re sponses to isotretinoin have been described. 3.2.3 Folliculiis Associated with HIV Infection Immune Recovery Inflammatory Folicults ‘The restoration of immune function with highly active antire- troviral therapy (HAART) can induce a regression of some skin problems. However, this restoration previously nonpathogenic infectious agents (i.e. D. folliewlorum, Pityrospo- ‘rum spp.) results in recognition of the agent by the immune system and may lead to the development of immune recovery inflamma- tory folliculitis in patients with a good immunologic res- ponse."""! The condition regresses alter topical corticosteroid therapy. ‘against 3.24 Skin Disorders with Follicular Expression ‘There are some skin disorders that ean produce a follicular eruption, Atopic dermatitis is one of these diseases and may present with widely dispersed prominent follicular papules. A form of psoriasis called follicular psoriasis," which occurs especially in children, presents as small desquamative follicular papules located mainly in the upper arms and the extension areas This condition may be confused with pityriasis rubra pilaris (fig- ure 8). There are some unusual reported cases of follicular sar- coidosis° 3.3 Pseudofolicults chronic inflammatory condition mainly observed in Black patients,"*"" is not a true folliculitis. The basis of its etiology is an inflammatory reaction that occurs after shav~ ing, when the sharp edge of the hair shaft transects the wall of the hair follicle or re-enters the epidermis. Papules and pustules in the beard distribution are the most common; however, other affected areas in predisposed individuals may include the scalp, axillae, ‘9 om Dateien BY Agr ates i. 8. Folicular psoriasis on the arm, Note the papulosquamous lesions \with folicutar distribution (confirmed by histopathotonc study). pubis, and legs. The most effective treatment seems to be laser hair removal using longer wavelengths." 4. Conclusions ‘The term folliculitis is used to describe a superficial inflamma- tion of the bair follicle, To ascertain the possible causes it is necessary to have wide clinical information with a complete physical examination. I is also important to ask about predispos- ing factors to cutancous infection. In order to clarify and simplify the spectrum of folliculitis, we have classified them into infectious and non-infectious folliculitis categories with clinical and thera- peutical comments, All the pustular Iesions should be cultured (bacterial, fungal or viral). Complementary studies can also be done in relation to clinical suspicion (HIV serology, syphilis, PCR cor biopsy), ‘There are many different types of non-infectious folliculitis, some of them with known etiology. The knowledge of these entities allows us to make a correct diagnosis and 10 provide specific treatment where possible. It should not be forgotten that there are skin diseases with follicular expression, such as atopic dermatitis or psoriasis. Acknowledgments No sources af funding were used to assist in the preparation ofthis review. “The author has no contiets of interest that are directly relevant to the content ofthis review, References Hogan P. Whats flicolits? Aust Fam Physician 199K: 27 (6) $289 (Chile K, Selkio BA, Morakawa Gd Skin microflora bacterial infections of the ‘skin, Imestg Dermatol Syenp Proc 2001: 6 (3): D0 Realy; teri nections ote sn, Prim Care 2000427 (2): 459-73 44 Zichchil, Asta, Not, Prsadomonas serginss flict er shower Tat J Dermatol 2000, 39 (3) 2104 Bhatia A, Brovell RT. Hott folic ext the water andthe patents for eudomonss, Posigrad Med 1999 106 (4) 43-6 Amn Dermat 28 55) Recognition and Management of Folhlitis 30 ”, x», ‘eien NK. The elinicsn’s choice of ani in the treatment of acter skin Infcton. Br J Denna 1998 139 3-8 Mikhail GR, Chapel TA. Follicle populopuslrsyphilid Arch Dermatol 1960 Jones HE, Reinhardt JH, Rnaldk MG. A cial msecogial an inmenoleseal survey of drmatophyess. rch Deoutal 1973 108: 61-8 ‘Smith KJ, Nea RC, Skelton IL] HG, etal. Majocei’s granuloma. J Cutan Patho 1991 18 (28°38 Bock O, Fuergemann J Horas Pyrospounfliculs: a common disease ofthe young and mide aged. J Ant Aead Dermatol 1985 12: 56-01 Ford GP. Ive FA, Migley G. iyrosponem foicliis and heloconsvle, Be ‘Dermatol 1982: 107 (6: 6918 Suse K, Vena, Sestoche C. Folic barhae caused by candi lca: esse reports. Micoes 199,42; 68355 Jang KA Kit ‘Viral floats onthe fae, Br J Dermal 2000; 12: Daft AL. Molina R Meret folliculitis, Cutan Med Surg 200261) 19-22 Schutte J, Myskowshi PL, Molluseum contagiosem in paints with human ‘mnmndfiieney ving nfcton: a review of tweaty seven patens. 7 An, ‘Acad Dermatol 1992; 77 5838 Weinberg IM, Tacamsky GW, Janes WD. Viral ficult. AIDS Patent Care STDS 198 13 0) 315.6 Ayres 8. Demeles fliculonum asa pathogen. Cats 1986; 37 (6: 44 shack RJ Fost ML, Nors AL. Papua ru erption of Dessdex falliculits in patents with acquired munodeficieney syndrome. Amn Acad Dern 1989; 21 300-7 Dominey A, Tecbeo J, Rosen T. Pyiasis fllculorum revised. J Am Acad i PlewigG, Jansen T. Acteiform dermatoses. Dermatology 1954; 195 (1: 102-7 Wakelin SH, Lipscombe T.Oron Da. Lihamrandcod flicularhyperker- test Chin Exp Dermal 196; 21 4) 29658 Deandea , Waller N, Mehimaber Meta, Demologicl reactions to hum: ‘erica evew of he literature. J Cin Psychopharmacol 1982; 23) 199-204, Berson ES. Reastions to anitubercalus drags [tr] J Invest Dermatol 1959; vs) Plewig G, Kigman AM. Vitamin A aid in acacform dermatoses, Acta Dorm ‘Venereol Sepp Stockh) 1975: 74: 119.27 Hosiges RE, Hood J, Canhom JE, etal. Clini mifestation of ascorbic seid deiieny in man. Am] Clin Nutr 1971 24 (8) 432-3 Frazier CN, Hu CK. Cutascous lesion associate wi eticeney in Vitamin in tan [ter], Arch niet Med 1931: 48 S07 Nichoer Actinic seria oliulis; a mcw entity? Br J Dermat 1985; 12: 6 Labanderra 3, Suarer-Campos A, Teibio J. Actinic superficial foliar J Dermat! 1998: 136 (63 1070-4 Collnick HP. Keatiein A. Topical weatment in ace: cumeat sts and fue spect. Derm 2005208 (1) 29.36 Lehman HP, Robinson KA, Andrews Il eal Acne therapy @ methatoigie veview-J Am Acad Derintl 2002 47 (2) 231-10 Leonard, Speting MC, Homoky C, eal Acne Kelodalis i form of primary ‘caring alopecia, Arch Dratol 200 Apr 136: 479-84 Luray M. Maor-Peres MA, et a. Acne keloid nchse an aed hai “oles, Demutology 1997: 194 (by. 713 ‘akock D, Foti HC, Bratn-Falso , Long lasing response to combined therapy ith favidic ac and rn, Asta Dermatol Vero (Stock 1992 72: 183-5 Walker SL, Sith HK, Lun K, etal Improvement of folic decalvans following shaving ofthe seal. Br} Dermatol 2000 Jum; 142 (6 1248-9 Powell J, Dawber RPR, Gar K. Folic dcavans inclding ted flicu Tis linia. slog and totapouse Nadings. Br J Dermat 198 140 383 Alley A. Al Hwssai K, Haine B, et al Two brothers with keratosis follicular spnuloa decane. 1 Am Acad Dermatol 2002; Sopp. $: 275-8 Rebor A. The ranagement of rosces, Ath J Clin Dermatol 2002; 3 (7: 49.96 Srlchee A. The link betwsen Helcobetr pylon infection and rsicen J Eur ‘Asad Darmatl Venera] 2002 Jul: 16 (4) 32833, Fostnger C. Kier H, Binder M. Treaunet of rosacea ike damodicioss with ‘al vermin ad topical permet cram. Am Acad Devt 19 Nov: G77 ‘9 om Dateien BY Agr ates 4s “8 *. sa 5 6 3. 8. oo. @. 3. 6. 6. 7. 6. 10. Koc K, Yogi 8, Valaposh Gta, Petia 5% cca vers metroniazsle (0.75% gel forthe teament of papulopustular rosacea: a randomized double bind plcebo contol stad, Dermatology 2002; 20 (3) 255-70 Lararos MC, Kerel FA. Topi terms Poti, Drags Toy (Bar) 2002 “an 38 (1): 7-18 Lande TA, Salven IN, Peso dermaits in children, Semin Caan Med Sarg 1999 Sep: 18 (3): 205) Jansen T. Pesoral demas suseesflly tres with peal adapaee, 3 Eur "Acad Dsematat Venerol 2002 Mar 16 2175-7 Giscobei R, Caro WA, Rochgh HHL FoxeFondyee ican. Arch Dermal 1979 TIS: 1368.6 Mil MIL, Hafod RR, Yeager IK, Fox-Foryce disease teat with tic clindangein slain. Arch Dent 1985 Oct: 131 (10 11128 bendy , Osos Happ R. FossFondye das na male patent response 1 alti wean Clin Exp Detaol 1994 Jan 19 (1): 67-9 (Che KM, Marshall MA, Marchal SF. Axilry Fox-Foniyee disease wate "with Hosuetion assed cuenage. Arch Dermatol 2002 Apr, 138 (482-40 obarman F.Fatet FR. Prt fallulis of pregnancy. Arch Dermal 1981: 17:20 ‘Spangler AS, Rely W, Hari WA. eta. Papular dermatitis of progancy: a 0 lnc eniy? JAMA 1962: Isl: S781 KrompourasG, Coen LM. Prt oliculitis of pregnancy. J Am Acad Dermatol 2k, 3: 132 ‘Ony} S, Opnio A, Horo, etal Fositopile pustular flew, Acta Derm YVenurel (Steck) 1970; 50: 195208 ‘Takematsa H, Nakawura K Tguash M, eal osinpilic pasar flu: ‘epor of two cses with & vow of the Japanese trate Arch Derm 1985. 121, 917-20 aaa T, Resell Jenes R, HIV-associated eosinophilic Flea: ene report ad review ofthe Uneratue. Br J Dermal 1996: 134 499-503, Sell, Leen E HIV-associated eosinophilic pustular folicuis: the fist ese reported in women, J Am Aca Demat 1995 35: 105-8 Faardfield LA, Rowe A, Frans N, etl ltchy folliculitis and human immune- ‘eficieney vis infection: eliicoathlogial am immanoloiel eats, pathogenesis and trestment. Br Dero 199% 13-1 (Garcia-Puos V.Pujl RM, De Mociga IM Iafaileeosiophie pustular liu Tis. Deramology 1994; 189; 296.9 Taleb A, BassrAndvcu L. et al Eosinepiie pusloss on the scalp ia ‘ildhood | Am Acad Deri 1992227 55-60 Lucimo-Agulr J, Sez-Anacho A, Foils posulos cosinalica ene tan. ‘hn Esp Poe 2001, 58: 184-8 Soxprono FF. Schinslla RA, Eosinophilic pasar follicle in pairs with Tequited nmmanedeicincy syne: report of axes cisex Am Acad Dermatol 1586: 1410202 Dale, Shaw J. Clinical pice, Bosnophie pestle fica. Lancet 2000; 396: 1238 Sato EE. Vesiculopasaardaeasey of neonates and infants. Cur Opin Pein 199: 64) 482.5 ‘Wagner A. Distinguishing vesicular and pustular dsonders in te nena. Carr ‘Opia Poli 1997: 9 (396405 Ginson LE, Muller SA, Leiferman KM. Folliclar mucinosis clinical apd is topathological stay J Amv Acad Dermatol 1989; 20 3) 441-8 Wilkinson JD, Black MIM, Chu A, Follicular mucinosis ascised with mycone fungoides resenting gros cyte changeson the face. Clin Fp Dermal 1982 73840 Vou Kobyltali G, Kreuer JA, Nome R, otal. Teeutmoat of opie Imocinossfliculitis wih UVAL eolé ight phototherapy. Dermatology 2000 2010 767 Yowsunawo 8, Uehimiya Hy Kanzaki TA case of folcular ovina weated ‘sicessfilly with minocjlin. Br J Desratol 2000 Ape: 12 (841-2 Krager K. Tebole B, Kengo Set a. Acquired reactive perforating demas: ‘successfilly weuted with allopurinol in 2 cases, Haart L999 Fe 30 (2) Ms20 Parson IW, Progress inthe perforating dermatoses, Arch Dermatol 1989: 128 ee) High M, Land HZ. Disseminate and cere nfndibuo-folicis repo ofa ‘xe, Arch Deel 1968 97 (4): 492-5 Ari K, Aivaits M,DavarisP, Disseminated ao recurent infunl bua folli Tis (DR) epot of ese seen ested with notin J Derm 99s. 25 (hes 13 Amn Dermat 28 55) 310 Lacino- Aguilar & Sabet Santandren 71, ouscrat F, Maubsc E, Materon Soa Toles AIDS 2000 1 3) 516.7 “72, Handa, Bingham JS. Demmsiological immune esvaion syndterme: does it “esis? rea Dem Venereol 200; 15 (9430-2 73. Oui 5, Uchara M Follicular erptions of sop demas. Arch Demat 1973; 07 547 74, Satake L, Even SWB. Follicular psoriasis. Be J Dermatol 1981; 104 153-6 1S. Fat K, Oka H, Ona Me a. Rect oil an icon pals sarcoidosis: or J Deratl 2000; 10): 303 76, Halder RM, Psudoflcuits rb and related disorders, Dero Clin 1988: 6 Geo Immne recovery inflammatory ‘csnnaAas Dotantermenon 8 Aagm retanes 77, Dun Jr JF, Psedeflliulis tac, Am Fam Physician 1988; 38; 169-78 18, Peny PK. Cookin FE, Raman 7, etal. Deisngpseoofolculkishabacin 2101: a eview of he erate andere tends Arn Aca Dermal 2002; 46:S1139 CCorresponclence and offprints: Dr jess Luelmo- Aguiar, Unitat de Dermato~ Jogi, Hospital cle Sabadell, Parc Taull, s/n, 08208 Sabadell, Spain, E-mail jlulmofespt.es Amn Dermat 28 55)

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