Scalp pruritus is a common dermatologic condition, but presents a challenge in diagnosis and treatment. A French epidemiologic study indicated that 21.49% of people older than 15 years have itching of the scalp as a symptom, and another US survey reported almost a 50% rate.1,2 Common scalp disorders such as seborrheic dermatitis (SD), psoriasis, tinea capitis, and pediculosis capitis all have a pruritic component.2,3 Bin Saif and colleagues categorize the origins of scalp itch into dermatologic, neuropathic, systemic, and psychogenic.4 The pathogenesis of itch in the scalp is a complex topic with a variety of factors such as histamines, leukotrienes, serotonin and opioids, neuropeptide SP, endothelin-1, thromboxane, prostaglandin, gastrin-related peptide, calcitonin gene-related peptide, cytokines, cannabinoids, and more.4,5 Microorganisms in the scalp, especially Malassezia species, also mediate pruritus.2-4
This multipart article will explore the common conditions that cause scalp itch and how to treat them in a clinical setting. Part I will address inflammatory dermatologic disorders, and Part II will discuss infectious dermatologic disorders, neuropathic, psychogenic, and systemic disorders.
Figure 1. Patients with psoriasis and scalp pruritus can experience lower work productivity, poor quality of sleep, and decreased emotional health.
Seborrheic Dermatitis
One of the major dermatologic conditions causing scalp itch is SD.4,6 The diagnosis is straightforward with scaling, erythema, and itching as the predominant presenting signs.7,8 About one-third to 50% of the population is affected by SD, which includes dandruff.7,8 The 3 groups that are most affected are infants younger than 3 months, adolescents in puberty, and adults between 40 to 60 years.8 SD should be suspected in immunocompromised patients such as AIDS, malignancies, or organ transplants.8 Patients with Parkinson disease and other neurologic disorders also have a higher prevalence rate.8
The mainstays of treatment are topical anti-inflammatory and antifungal medications (including selenium sulfide, zinc pyrithione, ketoconazole, and ciclopirox).8 Selenium sulfide and zinc can be used as first-line treatment when SD is predominately in the scalp (as dandruff).
Combination therapy with anti-inflammatories or antifungals can boost success rates in tougher cases.9 A recent Cochrane review ascertained that topical anti-inflammatory medications such as mild (class I or II) steroids and calcineurin inhibitors controlled SD.7 Both antifungals and steroids effectively produced short-term clearance, but strong steroids were better than azoles in reducing scaling, erythema, and itching.7 However, another Cochrane review of antifungals for SD found that ketoconazole had 44% lower side effects compared with steroids with both agents having equitable efficacy.10
Topical lithium gluconate, metronidazole, tar, UV-B phototherapy, and systemic antifungals (itraconazole and terbinafine) are also used.8 Systemic therapy is only warranted for disease refractory to topical treatment.8
One small Japanese study on patients affected by SD or psoriasis determined that scalp itch can decrease with appropriate hair-washing methods for more than 12 weeks.11 Detailed information about prewashing, washing with the shampoo (4 weeks of non-antibacterial shampoo, 4 weeks of antibacterial shampoo, and finally 4 weeks of the original non-antibacterial shampoo), rinsing, using conditioner, and drying were provided to the patients.11 At 8 and 12 weeks, there was statistically significant decreases in both scaling and itchiness coupled with decreased amount of total DNA of Malassezia species and bacteria in the scalp.11 Thus, instructing patients to wash hair properly should be an integral component of treatment combined with pharmaceutical therapy.
Psoriasis
Psoriasis is another common dermatologic condition in scalp pruritus.4,12 Itch in psoriasis can be a disconcerting symptom with increased burden due to lower work productivity, poor quality of sleep, and decreased emotional health12,13 (Figure 1). Up to 58% of patients with psoriasis may have scalp itch.12,14 Diagnosis of psoriasis is usually straightforward with characteristic silvery scaling papules and plaques on the body, usually in areas such as the scalp, extensor surfaces, and intergluteal cleft.13 Pruritus of psoriasis is generally cured with treatment of psoriatic lesions, but concomitant treatment of the itch is warranted.15
Mild scalp psoriasis is initially treated with topical vitamin D3 analogs and midpotency topical steroids.16 Moderate to severe disease should be treated with potent corticosteroids with an occlusive formulation, and possibly phototherapy.16 Systemic treatments should be considered for refractory disease.16 Capsaicin 0.025% cream can be used as a treatment for itch, but the face (and genitals) should be avoided.12 Topical treatments such as calcineurin inhibitors, salicylates, pramoxine (anesthetic), and crisaborole (Eucrisa; a topical phosphodiesterase 4 inhibitor) are possible options for itch.12
Currently, systemic therapies, especially biologics, are a major part of psoriasis treatment.12 Systemic therapy for psoriasis is indicated for high-intensity pruritus and for lesions in visible areas such as the scalp.17 Etanercept (Enbrel), ixekizumab (Taltz), ustekinumab (Stelara), and secukinumab (Cosentyx) are biologics with mean reduction of pruritus (using the itch numeric rating scale and visual analog scale) ranging from 3.6 to 5.2.12 A 4-point reduction in the itch numeric rating scale over a period of 12 weeks constitutes a true clinical change.18 Etanercept was the only therapy to fall below this 4-point change. Ixekizumab is possibly the best at reducing itch with an efficacy of 5.2, and significantly better than placebo or etanercept.12,19 The Janus kinase inhibitor tofacitinib (Xelijanz) at 10 mg twice daily reduced itch by 4.8 on the scale.12 Cyclosporin A also led to a decrease in eosinophils in the blood and pruritus in psoriasis.20
Mirtazapine at sub-antidepressant dosages (7.5-15 mg nightly) can treat psoriatic itch, particularly at bedtime.12 The antidepressants, doxepin (10-20 mg 3 times daily) and paroxetine (20 mg daily) are also possible options.15 Gabapentin and pregabalin are also efficacious in treating itch, but data specifically in psoriasis is lacking.12,15 Finally, narrowband UV-B phototherapy has shown efficacy in treating psoriatic scalp lesions and itch.12,15 However, common side effects of phototherapy are burning and itching, so some patients may not find a benefit from this treatment.13,21 Furthermore, hair can act as an obstacle for scalp psoriasis treatment, thus careful exposure and appropriate tools such as a laser hair comb may be necessary.22 Pruritus should be recognized as an important part of the psoriatic clinical picture, and treatment should be tailored to achieve control of both visual and nonvisual symptoms.
Geriatric Xerosis
The geriatric population has an increased propensity to be affected by pruritus.23-26 Data from 4099 patients (age >65 years) in a Turkish hospital over a 5-year period indicated pruritus affected 11.5% of admissions.24 Pruritus incidence increased with age with the group of 65 to 74 years at 10.3%, 75 to 84 years at 14.9%, and older than 85 years at 19.5%.24 Itch is higher in the fall (lower humidity) and lower in the spring (higher humidity).24
A prospective case-control study of geriatric patients with chronic idiopathic generalized pruritus compared with ethnicity and age-matched controls revealed possible differences in skin biophysical properties.23 Affected patients had lower surface sebum content on their forehead and increased baseline transepidermal water loss.23 As individuals age, they lose activity in sebaceous glands, sweat glands, and aquaphorin-3 (an important membrane channel for skin hydration).25,26
Corneodesmolysis is necessary for desquamation to replace older skin cells with newer ones from the basal layer.26 Improper or slowed corneodesmolysis is found in xerotic skin.26 Although a variety of disorders can cause itch in the elderly such as scabies, neurogenic, diabetes, systemic diseases (renal, liver disease, thyroid), hematologic malignancy, pharmaceutical side effects, iron deficiency, and more, we will focus on the most common disorder: xerosis.25 Nonetheless, disorders that can cause xerosis as a secondary factor such as HIV infection, nutritional deficiency, thyroid disease, diabetes, or malignancy should be on the differential.25,26
The geriatric population should eliminate any harsh soaps, detergents, or fabric softeners.25 Warm water should be used for short showers (<10 minutes), and moisturizers should be applied after a shower.25
Ointments especially inhibit evaporation, and offer occlusion and hydration due to elevated lipid content.25 Ammonium lactate 12% lotion and moisturizers act a keratolytic to aid in the corneodesmolysis process.26
Topical corticosteroids can also be useful, but should be used carefully to avoid side effects such as dermal atrophy.25,26 Topical calcineurin inhibitors might be better suited for a prolonged anti-inflammatory effect.25
Atopic Dermatitis
AD can present in the scalp, especially in the pediatric population.27 Although pruritus is a hallmark of AD, it may be hard to delineate in children younger than 2 years.27 Juicy papules, vesicles, and erythema are generally present in the face, trunk, and scalp.27 In 1 study, scaly scalp was seen in about 39% of patients with AD in the first year of life.28 In a study of the inpatient Chinese population with AD, scalp involvement occurred in 70% of infants (<2 years), 14.8% of children (2-12 years), 8.3% of adolescents (12-18 years), and 38.9% of adults (>18 years).29
For a select subset of patients younger than 5 years, avoiding potential trigger factors such as cow’s milk, eggs, wheat, soy, and peanuts is important.27,30 If patients have recalcitrant AD or a consistent history of flare ups after ingestion of a particular food, then food allergy evaluation is warrented.30 High-risk infants can also be bottle-fed partially or extensively hydrolyzed formula, according to the American Academy of Pediatrics.31 For older children and adults, pollen-related foods should be considered as allergic triggers.30 Aeroallergens such as dust mites, dander, and pollen serve as triggers with increasing prevalence as patients grow older.30
Application of moisturizers is paramount in managing AD in both adults and children.32 Moisturizers should be free of additives that may trigger flares such as fragrances and perfumes.32 Use of topical anti-inflammatory agents in infants should be relatively conservative compared with adults due to the higher ratio of body surface: body weight.27,32 Although there is a steroid phobia in parents, and perhaps even in providers, for using topical steroids in children, proper use results in effective and well-tolerated treatment.33,32 Hypothalamic-pituitary-adrenal axis suppression is possible, but rare with topical steroids.33 High-potency topical corticosteroids should be used only in the short term as an induction therapy for controlling disease.33 Moderate potency can be used for the trunk and extremities, and low potency in sensitive areas such as the face, neck, axilla, and genitals.33 The scalp is best treated with foams, solutions, oils, and gels.33 Wet wrap therapy coupled with a topical agent can increase penetration, and serve as a barrier to protect against excoriation.32 Twice-daily application might be necessary for older children and adults, but once daily can be sufficient for young children and infants.32
Topical calcineurin inhibitors are also acceptable for treatment in adults and pediatric populations.32 They can be considered especially in cases recalcitrant to steroids, for sensitive areas (face, neck, genitals), steroid-induced side effects, or combined with long-term use with topical steroids.32 Tacrolimus 0.03% can be used for ages 0 to15 years, and 0.1% for individuals older than 15 years32; twice-daily application is preferred.32 Some providers prefer to use off-label topical calcineurin inhibitors as first-line treatment in patients younger than 2 years.27,32 Maintenance therapy using either topical steroids (1-2 times weekly) or calcineurin inhibitors (2-3 times weekly) can reduce subsequent flare ups.30,32 Patients should be informed of potential cutaneous viral infections and possible malignancy associated with topical calcineurin inhibitors, but the actual risk based on existing data is unclear and probably minimal.32
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Bleach baths with intranasal mupirocin demonstrated clinical improvement in treating skin infections associated with AD; however, the clinical improvement was limited to skin submerged in the bath (ie, not the scalp or head).32 Phototherapy can be used to treat AD after failure of the previous treatments or as maintenance therapy.34 Physician-guided phototherapy is preferred to home phototherapy.34 There is no recommendation for a specific type of phototherapy; natural light, narrowband UV-B, broadband UV-B, and topical and systemic psoralen–UV-A are all feasible.34 Dosing should be based on minimal erythema dose and Fitzpatrick skin type.34 Phototherapy can be used as monotherapy or in conjunction with topical steroids.34 However, caution should be exercised with concomitant use with topical calcineurin inhibitors due to manufacturer warning.34 Phototherapy, especially narrowband UV-B, is generally considered safe in the pediatric population.34
If these previous methods fail, systemic therapy with cyclosporine, methotrexate, mycophenolate, and azathioprine can be used.34 However, limited data exists for strong recommendations on dosing, duration, and monitoring in AD.34 Existing general guidelines should be used for preliminary testing, use, monitoring, and adverse effects for systemic immunosuppressants.34 Clinicians must strive to use the lowest possible dosage in both adult and pediatric populations.34 Systemic steroids can be used, but only temporarily to resolve severe flare ups and as a bridge to other systemic therapies.34 Clinical correlation and patient specific treatment is advised.34 Omalizumab (Xolair) is a humanized monoclonal antibody, targeting the Fc receptor of IgE, FDA approved for asthma, and has demonstrated benefit in AD patients.34,35 The newly FDA-approved dupilumab (Dupixent), a humanized monocolonal antibody against IL-4α, has shown strong efficacy in treating moderate to severe AD.36 The most common treatment associated side effects were nasopharyngitis and headache.36 Trials are still ongoing for pediatric populations.36 Structured educational programs for patients and parents can be helpful in reducing disease burden and exacerbations, but require substantial monetary and temporal resources.30
Contact Dermatitis
Contact dermatitis (CD) of the scalp is another source of pruritus. A study of 1320 patch tested patients (for scalp allergic CD) in the Information Network of Departments of Dermatology (IVDK; between 1993 and 2003) revealed hair-coloring agents were the most common allergens causing sensitization.37
The main (commercial patch testing) agents were p-phenylenediamine, tolune-2,5-diamine, p-aminophenol, 3-aminophenol, p-aminoazobenzene, cocamidopropyl betaine, and pyrogallol and caused significantly higher sensitization compared with the remaining IVDK patients.37 Of the study population, 78% were women, but this may be due to over half of all women in industrial nations using hair-coloring substances.37 Patients’ personal products were also tested in 690 patients and revealed that medical products, hair tints, bleaches, and hair-cleansing products caused two-thirds of positive tests in this subgroup.37 Hair tints and bleaches were the most likely culprit, and more than 80% of these patients did not react to an allergen in the commercial patch test.37 Therefore, for a patient who may have allergic CD of the scalp, both commercial patch testing and the patient’s own products is imperative.37Thioglycolate, formaldehyde, lanolin, fragrances, solvents, and surfactants are also possible allergens in cosmetic hair prodcuts.38 Adhesive in hair extension and wigs and topical drugs (such as minoxidil and its the solvent propylene glycol) are possible.39 The chemicals listed are not exhaustive as a variety can trigger an allergic response.39 Affected patients may have pruritus, vesicles, papules, pustules, edema, and erythema on the scalp, but also on the face, neck, and other adjacent areas that the allergen affected.39,40
Irritant CD is also possible with no prerequisite sensitization, and may be more common than its allergic counterpart.38,41 Detergents, shampoo (especially ones with sodium lauryl sulfate), and a variety of entities can cause irritant CD.41 Patients have stinging pain, itching, burning, erythema, and edema.38,40 Although both allergic and irritant CD can cause pruritus, the allergic pruritus is much worse.40 Allergic CD may have more distinct borders and geometrical demarcation, while irritant CD has less distinct borders.40
Treatment for both allergic and CD involves diagnosing the condition and determining the responsible substance.40,41 Cessation and prevention of exposure is the ideal course.40,41 For localized CD, topical mid- to high-potency steroids can offer relief. If sensitive areas (face, eyelids, neck) are included, then a low-potency steroid like desonide should be used.40,41 For CD that involves greater than 20% of the skin or for severe cases, systemic steroid therapy can be prescribed.40,41
Figure 2. Patients with alopecia can experience hair loss and scalp pruritus.
Cicatricial Alopecias
Cicatricial alopecias are a known source of pruritus of the scalp42 (Figure 2). Chronic cutaneous lupus erythematous, especially the form discoid lupus erythematous (DLE) which constitutes 50% to 85% of cases, presents with pruritus, pain, scaling, erythema, and discoloration of the affected scalp.42,43
DLE affects is more prone in women, and cases in African Americans can be more severe.42,43 Limiting sun exposure and wearing sunscreens are part of the preventive treatment.
Topical and intralesional corticosteroids, calcineurin inhibitors, and hydroxychloroquine are the mainstays of treatment.42 Rapidly progressive disease should be treated with hydroxychloroquine first, and slowly progressive disease should be first treated with corticosteroids.43 Oral retinoids are also a possible choice.43 Systemic immunosuppressive therapy may be warranted for severe and generalized disease.42,43
Lichen planopilaris (LPP) and its subtypes classic, frontal fibrosing alopecia (FFA), and Graham Little syndrome are rare cicatricial alopecias.42 LPP usually affects adult women in the crown and parietal areas with generalized or focal areas of disease.42 FFA affects postmenopausal women with a band-like hair loss at the frontal hair line and the eyebrows.42 Graham Little syndrome presents with cicatricial alopecia of the scalp, lichen planus spinulosus, and noncicatricial alopecia of pubic and axillary regions.42 Follicular hyperkeratosis and perilesional erythema are found clinically in all forms of LPP.43 Topical and intralesional steroids are used along with hydroxychloroquine. Cyclosporine and mycophenolate mofetil are used in refractory cases.42 Topical minoxidil can abate further hair loss.42
Central centrifugal cicatricial alopecia is a permanent scarring hair loss predominately affecting African American women. Patients experience pain, burning, and pruritus. The alopecia starts at the vertex and expands symmetrically. As with other cicatricial alopecias anti-inflammatory treatment is first line to reduce progression. Topical and intralesional corticosteroids, topical calcineurin inhibitors, and oral tetracyclines are used. Topical minoxidil is also used promote hair growth.42
Conclusion
Diagnosing the source of scalp pruritus is critical in treating these inflammatory dermatologic disorders. While AD might present with pruritus as one of the most severe symptoms, diseases like psoriasis or cicatricial alopecias might have other symptoms that confound the impact of itching. Dermatologists must be aware and vigilant in treating scalp pruritus.
Mr Subash is a research fellow in the department of dermatology at Wake Forest Baptist Health in Winston-Salem, NC.
Dr McMichael, The Mane Point Section Editor, is professor and chair in the department of dermatology at Wake Forest Baptist Health in Winston-Salem, NC.
Disclosure: Dr McMichael has received grants from Allergan and Proctor & Gamble. She is a consultant for Allergan, eResearch Technology, Inc, Galderma, Guthey Renker, Johnson & Johnson, Keranetics, Merck & Co, Inc, Merz Pharmaceuticals, Proctor & Gamble, Samumed, and Incyte. She receives royalties from Informa Healthcare and UpToDate and also has conducted research for Samumed.
Mr Subash reports no relevant financial relationships.
References
1. Misery L, Rahhali N, Duhamel A, Taieb C. Epidemiology of dandruff, scalp pruritus and associated symptoms. Acta Derm Venereol. 2013;93(1):80-81.
2. Elewski BE. Clinical diagnosis of common scalp disorders. J Investig Dermatol Symp Proc. 2005;10(3):190-193.
3. Grimalt R. A practical guide to scalp disorders. J Investig Dermatol Symp Proc. 2007;12(2):10-14.
4. Bin Saif GA, Ericson ME, Yosipovitch G. The itchy scalp–scratching for an explanation. Exp Dermatol. 2011;20(12):959-968.
5. Reamy BV, Bunt CW, Fletcher S. A diagnostic approach to pruritus. Am Fam Physician. 2011;84(2):195-202.
6. Dall’Oglio F, Lacarrubba F, Verzì AE, Micali G. Noncorticosteroid combination shampoo versus 1% ketoconazole shampoo for the management of mild-to-moderate seborrheic dermatitis of the scalp: results from a randomized, investigator-single-blind trial using clinical and trichoscopic evaluation. Skin Appendage Disord. 2016;1(3):126-130.
7. Kastarinen H, Oksanen T, Okokon EO, et al. Topical anti-inflammatory agents for seborrheic dermatitis of the face or scalp. Cochrane Database Syst Rev. 2014;(5):CD009446. doi:10.1002/14651858.CD009446.pub2
8. Borda LJ, Wikramanayake TC. Seborrheic dermatitis and dandruff: a comprehensive review. J Clin Investig Dermatol. 2015;3(2).
9. Berk T, Scheinfeld N. Seborrheic dermatitis. P T. 2010;35(6):348-352.
10. Okokon EO, Verbeek JH, Ruotsalainen JH, Ojo OA, Bakhoya VN. Topical antifungals for seborrhoeic dermatitis. Cochrane Database Syst Rev. 2015;(5):CD008138. doi:10.1002/14651858.CD008138.pub3
11. Kobayashi M, Ito K, Sugita T, et al. Physiological and microbiological verification of the benefit of hair washing in patients with skin conditions of the scalp. J Cosmet Dermatol. 2016;15(4):e1-e8.
12. Stull C, Grossman S, Yosipovitch G. Current and emerging therapies for itch management in psoriasis. Am J Clin Dermatol. 2016;17(6):617-624.
13. Szepietowski JC, Reich A. Pruritus in psoriasis: An update. Eur J Pain. 2016;20(1):41-46.
14. O’Neill JL, Chan YH, Rapp SR, Yosipovitch G. Differences in itch characteristics between psoriasis and atopic dermatitis patients: results of a web-based questionnaire. Acta Derm Venereol. 2011;91(5):537-540.
15. Reich A, Szepietowski JC. Clinical aspects of itch: psoriasis. In: Carstens E, Akiyama T, eds. Itch: Mechanisms and Treatment. Boca Raton, FL: CRC Press; 2014:chap 4.
16. Ortonne J, Chimenti S, Luger T, Puig L, Reid F, Trüeb RM. Scalp psoriasis: European consensus on grading and treatment algorithm. J Eur Acad Dermatol Venereol. 2009;23(12):1435-1444.
17. Gisondi P, Di Mercurio M, Idolazzi L, Girolomoni G. Concept of remission in chronic plaque psoriasis. J Rheumatol Suppl. 2015;93:57-60.
18. Kimball AB, Naegeli AN, Edson-Heredia E, et al. Psychometric properties of the itch numeric rating scale in patients with moderate-to-severe plaque psoriasis. Br J Dermatol. 2016;175(1):157-162.
19. Kimball AB, Luger T, Gottlieb A, et al. Impact of ixekizumab on psoriasis itch severity and other psoriasis symptoms: results from 3 phase III psoriasis clinical trials. J Am Acad Dermatol. 2016;75(6):1156-1161.
20. Schopf RE, Hultsch T, Lotz J, Bräutigam M. Eosinophils, pruritus and psoriasis: effects of treatment with etretinate or cyclosporin-A. J Eur Acad Dermatol Venereol. 1998;11(3):234-239.
Scalp pruritus is a common dermatologic condition, but presents a challenge in diagnosis and treatment. A French epidemiologic study indicated that 21.49% of people older than 15 years have itching of the scalp as a symptom, and another US survey reported almost a 50% rate.1,2 Common scalp disorders such as seborrheic dermatitis (SD), psoriasis, tinea capitis, and pediculosis capitis all have a pruritic component.2,3 Bin Saif and colleagues categorize the origins of scalp itch into dermatologic, neuropathic, systemic, and psychogenic.4 The pathogenesis of itch in the scalp is a complex topic with a variety of factors such as histamines, leukotrienes, serotonin and opioids, neuropeptide SP, endothelin-1, thromboxane, prostaglandin, gastrin-related peptide, calcitonin gene-related peptide, cytokines, cannabinoids, and more.4,5 Microorganisms in the scalp, especially Malassezia species, also mediate pruritus.2-4
This multipart article will explore the common conditions that cause scalp itch and how to treat them in a clinical setting. Part I will address inflammatory dermatologic disorders, and Part II will discuss infectious dermatologic disorders, neuropathic, psychogenic, and systemic disorders.
Figure 1. Patients with psoriasis and scalp pruritus can experience lower work productivity, poor quality of sleep, and decreased emotional health.
Seborrheic Dermatitis
One of the major dermatologic conditions causing scalp itch is SD.4,6 The diagnosis is straightforward with scaling, erythema, and itching as the predominant presenting signs.7,8 About one-third to 50% of the population is affected by SD, which includes dandruff.7,8 The 3 groups that are most affected are infants younger than 3 months, adolescents in puberty, and adults between 40 to 60 years.8 SD should be suspected in immunocompromised patients such as AIDS, malignancies, or organ transplants.8 Patients with Parkinson disease and other neurologic disorders also have a higher prevalence rate.8
The mainstays of treatment are topical anti-inflammatory and antifungal medications (including selenium sulfide, zinc pyrithione, ketoconazole, and ciclopirox).8 Selenium sulfide and zinc can be used as first-line treatment when SD is predominately in the scalp (as dandruff).
Combination therapy with anti-inflammatories or antifungals can boost success rates in tougher cases.9 A recent Cochrane review ascertained that topical anti-inflammatory medications such as mild (class I or II) steroids and calcineurin inhibitors controlled SD.7 Both antifungals and steroids effectively produced short-term clearance, but strong steroids were better than azoles in reducing scaling, erythema, and itching.7 However, another Cochrane review of antifungals for SD found that ketoconazole had 44% lower side effects compared with steroids with both agents having equitable efficacy.10
Topical lithium gluconate, metronidazole, tar, UV-B phototherapy, and systemic antifungals (itraconazole and terbinafine) are also used.8 Systemic therapy is only warranted for disease refractory to topical treatment.8
One small Japanese study on patients affected by SD or psoriasis determined that scalp itch can decrease with appropriate hair-washing methods for more than 12 weeks.11 Detailed information about prewashing, washing with the shampoo (4 weeks of non-antibacterial shampoo, 4 weeks of antibacterial shampoo, and finally 4 weeks of the original non-antibacterial shampoo), rinsing, using conditioner, and drying were provided to the patients.11 At 8 and 12 weeks, there was statistically significant decreases in both scaling and itchiness coupled with decreased amount of total DNA of Malassezia species and bacteria in the scalp.11 Thus, instructing patients to wash hair properly should be an integral component of treatment combined with pharmaceutical therapy.
Psoriasis
Psoriasis is another common dermatologic condition in scalp pruritus.4,12 Itch in psoriasis can be a disconcerting symptom with increased burden due to lower work productivity, poor quality of sleep, and decreased emotional health12,13 (Figure 1). Up to 58% of patients with psoriasis may have scalp itch.12,14 Diagnosis of psoriasis is usually straightforward with characteristic silvery scaling papules and plaques on the body, usually in areas such as the scalp, extensor surfaces, and intergluteal cleft.13 Pruritus of psoriasis is generally cured with treatment of psoriatic lesions, but concomitant treatment of the itch is warranted.15
Mild scalp psoriasis is initially treated with topical vitamin D3 analogs and midpotency topical steroids.16 Moderate to severe disease should be treated with potent corticosteroids with an occlusive formulation, and possibly phototherapy.16 Systemic treatments should be considered for refractory disease.16 Capsaicin 0.025% cream can be used as a treatment for itch, but the face (and genitals) should be avoided.12 Topical treatments such as calcineurin inhibitors, salicylates, pramoxine (anesthetic), and crisaborole (Eucrisa; a topical phosphodiesterase 4 inhibitor) are possible options for itch.12
Currently, systemic therapies, especially biologics, are a major part of psoriasis treatment.12 Systemic therapy for psoriasis is indicated for high-intensity pruritus and for lesions in visible areas such as the scalp.17 Etanercept (Enbrel), ixekizumab (Taltz), ustekinumab (Stelara), and secukinumab (Cosentyx) are biologics with mean reduction of pruritus (using the itch numeric rating scale and visual analog scale) ranging from 3.6 to 5.2.12 A 4-point reduction in the itch numeric rating scale over a period of 12 weeks constitutes a true clinical change.18 Etanercept was the only therapy to fall below this 4-point change. Ixekizumab is possibly the best at reducing itch with an efficacy of 5.2, and significantly better than placebo or etanercept.12,19 The Janus kinase inhibitor tofacitinib (Xelijanz) at 10 mg twice daily reduced itch by 4.8 on the scale.12 Cyclosporin A also led to a decrease in eosinophils in the blood and pruritus in psoriasis.20
Mirtazapine at sub-antidepressant dosages (7.5-15 mg nightly) can treat psoriatic itch, particularly at bedtime.12 The antidepressants, doxepin (10-20 mg 3 times daily) and paroxetine (20 mg daily) are also possible options.15 Gabapentin and pregabalin are also efficacious in treating itch, but data specifically in psoriasis is lacking.12,15 Finally, narrowband UV-B phototherapy has shown efficacy in treating psoriatic scalp lesions and itch.12,15 However, common side effects of phototherapy are burning and itching, so some patients may not find a benefit from this treatment.13,21 Furthermore, hair can act as an obstacle for scalp psoriasis treatment, thus careful exposure and appropriate tools such as a laser hair comb may be necessary.22 Pruritus should be recognized as an important part of the psoriatic clinical picture, and treatment should be tailored to achieve control of both visual and nonvisual symptoms.
Geriatric Xerosis
The geriatric population has an increased propensity to be affected by pruritus.23-26 Data from 4099 patients (age >65 years) in a Turkish hospital over a 5-year period indicated pruritus affected 11.5% of admissions.24 Pruritus incidence increased with age with the group of 65 to 74 years at 10.3%, 75 to 84 years at 14.9%, and older than 85 years at 19.5%.24 Itch is higher in the fall (lower humidity) and lower in the spring (higher humidity).24
A prospective case-control study of geriatric patients with chronic idiopathic generalized pruritus compared with ethnicity and age-matched controls revealed possible differences in skin biophysical properties.23 Affected patients had lower surface sebum content on their forehead and increased baseline transepidermal water loss.23 As individuals age, they lose activity in sebaceous glands, sweat glands, and aquaphorin-3 (an important membrane channel for skin hydration).25,26
Corneodesmolysis is necessary for desquamation to replace older skin cells with newer ones from the basal layer.26 Improper or slowed corneodesmolysis is found in xerotic skin.26 Although a variety of disorders can cause itch in the elderly such as scabies, neurogenic, diabetes, systemic diseases (renal, liver disease, thyroid), hematologic malignancy, pharmaceutical side effects, iron deficiency, and more, we will focus on the most common disorder: xerosis.25 Nonetheless, disorders that can cause xerosis as a secondary factor such as HIV infection, nutritional deficiency, thyroid disease, diabetes, or malignancy should be on the differential.25,26
The geriatric population should eliminate any harsh soaps, detergents, or fabric softeners.25 Warm water should be used for short showers (<10 minutes), and moisturizers should be applied after a shower.25
Ointments especially inhibit evaporation, and offer occlusion and hydration due to elevated lipid content.25 Ammonium lactate 12% lotion and moisturizers act a keratolytic to aid in the corneodesmolysis process.26
Topical corticosteroids can also be useful, but should be used carefully to avoid side effects such as dermal atrophy.25,26 Topical calcineurin inhibitors might be better suited for a prolonged anti-inflammatory effect.25
Atopic Dermatitis
AD can present in the scalp, especially in the pediatric population.27 Although pruritus is a hallmark of AD, it may be hard to delineate in children younger than 2 years.27 Juicy papules, vesicles, and erythema are generally present in the face, trunk, and scalp.27 In 1 study, scaly scalp was seen in about 39% of patients with AD in the first year of life.28 In a study of the inpatient Chinese population with AD, scalp involvement occurred in 70% of infants (<2 years), 14.8% of children (2-12 years), 8.3% of adolescents (12-18 years), and 38.9% of adults (>18 years).29
For a select subset of patients younger than 5 years, avoiding potential trigger factors such as cow’s milk, eggs, wheat, soy, and peanuts is important.27,30 If patients have recalcitrant AD or a consistent history of flare ups after ingestion of a particular food, then food allergy evaluation is warrented.30 High-risk infants can also be bottle-fed partially or extensively hydrolyzed formula, according to the American Academy of Pediatrics.31 For older children and adults, pollen-related foods should be considered as allergic triggers.30 Aeroallergens such as dust mites, dander, and pollen serve as triggers with increasing prevalence as patients grow older.30
Application of moisturizers is paramount in managing AD in both adults and children.32 Moisturizers should be free of additives that may trigger flares such as fragrances and perfumes.32 Use of topical anti-inflammatory agents in infants should be relatively conservative compared with adults due to the higher ratio of body surface: body weight.27,32 Although there is a steroid phobia in parents, and perhaps even in providers, for using topical steroids in children, proper use results in effective and well-tolerated treatment.33,32 Hypothalamic-pituitary-adrenal axis suppression is possible, but rare with topical steroids.33 High-potency topical corticosteroids should be used only in the short term as an induction therapy for controlling disease.33 Moderate potency can be used for the trunk and extremities, and low potency in sensitive areas such as the face, neck, axilla, and genitals.33 The scalp is best treated with foams, solutions, oils, and gels.33 Wet wrap therapy coupled with a topical agent can increase penetration, and serve as a barrier to protect against excoriation.32 Twice-daily application might be necessary for older children and adults, but once daily can be sufficient for young children and infants.32
Topical calcineurin inhibitors are also acceptable for treatment in adults and pediatric populations.32 They can be considered especially in cases recalcitrant to steroids, for sensitive areas (face, neck, genitals), steroid-induced side effects, or combined with long-term use with topical steroids.32 Tacrolimus 0.03% can be used for ages 0 to15 years, and 0.1% for individuals older than 15 years32; twice-daily application is preferred.32 Some providers prefer to use off-label topical calcineurin inhibitors as first-line treatment in patients younger than 2 years.27,32 Maintenance therapy using either topical steroids (1-2 times weekly) or calcineurin inhibitors (2-3 times weekly) can reduce subsequent flare ups.30,32 Patients should be informed of potential cutaneous viral infections and possible malignancy associated with topical calcineurin inhibitors, but the actual risk based on existing data is unclear and probably minimal.32
Article continues on page 2
Bleach baths with intranasal mupirocin demonstrated clinical improvement in treating skin infections associated with AD; however, the clinical improvement was limited to skin submerged in the bath (ie, not the scalp or head).32 Phototherapy can be used to treat AD after failure of the previous treatments or as maintenance therapy.34 Physician-guided phototherapy is preferred to home phototherapy.34 There is no recommendation for a specific type of phototherapy; natural light, narrowband UV-B, broadband UV-B, and topical and systemic psoralen–UV-A are all feasible.34 Dosing should be based on minimal erythema dose and Fitzpatrick skin type.34 Phototherapy can be used as monotherapy or in conjunction with topical steroids.34 However, caution should be exercised with concomitant use with topical calcineurin inhibitors due to manufacturer warning.34 Phototherapy, especially narrowband UV-B, is generally considered safe in the pediatric population.34
If these previous methods fail, systemic therapy with cyclosporine, methotrexate, mycophenolate, and azathioprine can be used.34 However, limited data exists for strong recommendations on dosing, duration, and monitoring in AD.34 Existing general guidelines should be used for preliminary testing, use, monitoring, and adverse effects for systemic immunosuppressants.34 Clinicians must strive to use the lowest possible dosage in both adult and pediatric populations.34 Systemic steroids can be used, but only temporarily to resolve severe flare ups and as a bridge to other systemic therapies.34 Clinical correlation and patient specific treatment is advised.34 Omalizumab (Xolair) is a humanized monoclonal antibody, targeting the Fc receptor of IgE, FDA approved for asthma, and has demonstrated benefit in AD patients.34,35 The newly FDA-approved dupilumab (Dupixent), a humanized monocolonal antibody against IL-4α, has shown strong efficacy in treating moderate to severe AD.36 The most common treatment associated side effects were nasopharyngitis and headache.36 Trials are still ongoing for pediatric populations.36 Structured educational programs for patients and parents can be helpful in reducing disease burden and exacerbations, but require substantial monetary and temporal resources.30
Contact Dermatitis
Contact dermatitis (CD) of the scalp is another source of pruritus. A study of 1320 patch tested patients (for scalp allergic CD) in the Information Network of Departments of Dermatology (IVDK; between 1993 and 2003) revealed hair-coloring agents were the most common allergens causing sensitization.37
The main (commercial patch testing) agents were p-phenylenediamine, tolune-2,5-diamine, p-aminophenol, 3-aminophenol, p-aminoazobenzene, cocamidopropyl betaine, and pyrogallol and caused significantly higher sensitization compared with the remaining IVDK patients.37 Of the study population, 78% were women, but this may be due to over half of all women in industrial nations using hair-coloring substances.37 Patients’ personal products were also tested in 690 patients and revealed that medical products, hair tints, bleaches, and hair-cleansing products caused two-thirds of positive tests in this subgroup.37 Hair tints and bleaches were the most likely culprit, and more than 80% of these patients did not react to an allergen in the commercial patch test.37 Therefore, for a patient who may have allergic CD of the scalp, both commercial patch testing and the patient’s own products is imperative.37Thioglycolate, formaldehyde, lanolin, fragrances, solvents, and surfactants are also possible allergens in cosmetic hair prodcuts.38 Adhesive in hair extension and wigs and topical drugs (such as minoxidil and its the solvent propylene glycol) are possible.39 The chemicals listed are not exhaustive as a variety can trigger an allergic response.39 Affected patients may have pruritus, vesicles, papules, pustules, edema, and erythema on the scalp, but also on the face, neck, and other adjacent areas that the allergen affected.39,40
Irritant CD is also possible with no prerequisite sensitization, and may be more common than its allergic counterpart.38,41 Detergents, shampoo (especially ones with sodium lauryl sulfate), and a variety of entities can cause irritant CD.41 Patients have stinging pain, itching, burning, erythema, and edema.38,40 Although both allergic and irritant CD can cause pruritus, the allergic pruritus is much worse.40 Allergic CD may have more distinct borders and geometrical demarcation, while irritant CD has less distinct borders.40
Treatment for both allergic and CD involves diagnosing the condition and determining the responsible substance.40,41 Cessation and prevention of exposure is the ideal course.40,41 For localized CD, topical mid- to high-potency steroids can offer relief. If sensitive areas (face, eyelids, neck) are included, then a low-potency steroid like desonide should be used.40,41 For CD that involves greater than 20% of the skin or for severe cases, systemic steroid therapy can be prescribed.40,41
Figure 2. Patients with alopecia can experience hair loss and scalp pruritus.
Cicatricial Alopecias
Cicatricial alopecias are a known source of pruritus of the scalp42 (Figure 2). Chronic cutaneous lupus erythematous, especially the form discoid lupus erythematous (DLE) which constitutes 50% to 85% of cases, presents with pruritus, pain, scaling, erythema, and discoloration of the affected scalp.42,43
DLE affects is more prone in women, and cases in African Americans can be more severe.42,43 Limiting sun exposure and wearing sunscreens are part of the preventive treatment.
Topical and intralesional corticosteroids, calcineurin inhibitors, and hydroxychloroquine are the mainstays of treatment.42 Rapidly progressive disease should be treated with hydroxychloroquine first, and slowly progressive disease should be first treated with corticosteroids.43 Oral retinoids are also a possible choice.43 Systemic immunosuppressive therapy may be warranted for severe and generalized disease.42,43
Lichen planopilaris (LPP) and its subtypes classic, frontal fibrosing alopecia (FFA), and Graham Little syndrome are rare cicatricial alopecias.42 LPP usually affects adult women in the crown and parietal areas with generalized or focal areas of disease.42 FFA affects postmenopausal women with a band-like hair loss at the frontal hair line and the eyebrows.42 Graham Little syndrome presents with cicatricial alopecia of the scalp, lichen planus spinulosus, and noncicatricial alopecia of pubic and axillary regions.42 Follicular hyperkeratosis and perilesional erythema are found clinically in all forms of LPP.43 Topical and intralesional steroids are used along with hydroxychloroquine. Cyclosporine and mycophenolate mofetil are used in refractory cases.42 Topical minoxidil can abate further hair loss.42
Central centrifugal cicatricial alopecia is a permanent scarring hair loss predominately affecting African American women. Patients experience pain, burning, and pruritus. The alopecia starts at the vertex and expands symmetrically. As with other cicatricial alopecias anti-inflammatory treatment is first line to reduce progression. Topical and intralesional corticosteroids, topical calcineurin inhibitors, and oral tetracyclines are used. Topical minoxidil is also used promote hair growth.42
Conclusion
Diagnosing the source of scalp pruritus is critical in treating these inflammatory dermatologic disorders. While AD might present with pruritus as one of the most severe symptoms, diseases like psoriasis or cicatricial alopecias might have other symptoms that confound the impact of itching. Dermatologists must be aware and vigilant in treating scalp pruritus.
Mr Subash is a research fellow in the department of dermatology at Wake Forest Baptist Health in Winston-Salem, NC.
Dr McMichael, The Mane Point Section Editor, is professor and chair in the department of dermatology at Wake Forest Baptist Health in Winston-Salem, NC.
Disclosure: Dr McMichael has received grants from Allergan and Proctor & Gamble. She is a consultant for Allergan, eResearch Technology, Inc, Galderma, Guthey Renker, Johnson & Johnson, Keranetics, Merck & Co, Inc, Merz Pharmaceuticals, Proctor & Gamble, Samumed, and Incyte. She receives royalties from Informa Healthcare and UpToDate and also has conducted research for Samumed.
Mr Subash reports no relevant financial relationships.
References
1. Misery L, Rahhali N, Duhamel A, Taieb C. Epidemiology of dandruff, scalp pruritus and associated symptoms. Acta Derm Venereol. 2013;93(1):80-81.
2. Elewski BE. Clinical diagnosis of common scalp disorders. J Investig Dermatol Symp Proc. 2005;10(3):190-193.
3. Grimalt R. A practical guide to scalp disorders. J Investig Dermatol Symp Proc. 2007;12(2):10-14.
4. Bin Saif GA, Ericson ME, Yosipovitch G. The itchy scalp–scratching for an explanation. Exp Dermatol. 2011;20(12):959-968.
5. Reamy BV, Bunt CW, Fletcher S. A diagnostic approach to pruritus. Am Fam Physician. 2011;84(2):195-202.
6. Dall’Oglio F, Lacarrubba F, Verzì AE, Micali G. Noncorticosteroid combination shampoo versus 1% ketoconazole shampoo for the management of mild-to-moderate seborrheic dermatitis of the scalp: results from a randomized, investigator-single-blind trial using clinical and trichoscopic evaluation. Skin Appendage Disord. 2016;1(3):126-130.
7. Kastarinen H, Oksanen T, Okokon EO, et al. Topical anti-inflammatory agents for seborrheic dermatitis of the face or scalp. Cochrane Database Syst Rev. 2014;(5):CD009446. doi:10.1002/14651858.CD009446.pub2
8. Borda LJ, Wikramanayake TC. Seborrheic dermatitis and dandruff: a comprehensive review. J Clin Investig Dermatol. 2015;3(2).
9. Berk T, Scheinfeld N. Seborrheic dermatitis. P T. 2010;35(6):348-352.
10. Okokon EO, Verbeek JH, Ruotsalainen JH, Ojo OA, Bakhoya VN. Topical antifungals for seborrhoeic dermatitis. Cochrane Database Syst Rev. 2015;(5):CD008138. doi:10.1002/14651858.CD008138.pub3
11. Kobayashi M, Ito K, Sugita T, et al. Physiological and microbiological verification of the benefit of hair washing in patients with skin conditions of the scalp. J Cosmet Dermatol. 2016;15(4):e1-e8.
12. Stull C, Grossman S, Yosipovitch G. Current and emerging therapies for itch management in psoriasis. Am J Clin Dermatol. 2016;17(6):617-624.
13. Szepietowski JC, Reich A. Pruritus in psoriasis: An update. Eur J Pain. 2016;20(1):41-46.
14. O’Neill JL, Chan YH, Rapp SR, Yosipovitch G. Differences in itch characteristics between psoriasis and atopic dermatitis patients: results of a web-based questionnaire. Acta Derm Venereol. 2011;91(5):537-540.
15. Reich A, Szepietowski JC. Clinical aspects of itch: psoriasis. In: Carstens E, Akiyama T, eds. Itch: Mechanisms and Treatment. Boca Raton, FL: CRC Press; 2014:chap 4.
16. Ortonne J, Chimenti S, Luger T, Puig L, Reid F, Trüeb RM. Scalp psoriasis: European consensus on grading and treatment algorithm. J Eur Acad Dermatol Venereol. 2009;23(12):1435-1444.
17. Gisondi P, Di Mercurio M, Idolazzi L, Girolomoni G. Concept of remission in chronic plaque psoriasis. J Rheumatol Suppl. 2015;93:57-60.
18. Kimball AB, Naegeli AN, Edson-Heredia E, et al. Psychometric properties of the itch numeric rating scale in patients with moderate-to-severe plaque psoriasis. Br J Dermatol. 2016;175(1):157-162.
19. Kimball AB, Luger T, Gottlieb A, et al. Impact of ixekizumab on psoriasis itch severity and other psoriasis symptoms: results from 3 phase III psoriasis clinical trials. J Am Acad Dermatol. 2016;75(6):1156-1161.
20. Schopf RE, Hultsch T, Lotz J, Bräutigam M. Eosinophils, pruritus and psoriasis: effects of treatment with etretinate or cyclosporin-A. J Eur Acad Dermatol Venereol. 1998;11(3):234-239.
Scalp pruritus is a common dermatologic condition, but presents a challenge in diagnosis and treatment. A French epidemiologic study indicated that 21.49% of people older than 15 years have itching of the scalp as a symptom, and another US survey reported almost a 50% rate.1,2 Common scalp disorders such as seborrheic dermatitis (SD), psoriasis, tinea capitis, and pediculosis capitis all have a pruritic component.2,3 Bin Saif and colleagues categorize the origins of scalp itch into dermatologic, neuropathic, systemic, and psychogenic.4 The pathogenesis of itch in the scalp is a complex topic with a variety of factors such as histamines, leukotrienes, serotonin and opioids, neuropeptide SP, endothelin-1, thromboxane, prostaglandin, gastrin-related peptide, calcitonin gene-related peptide, cytokines, cannabinoids, and more.4,5 Microorganisms in the scalp, especially Malassezia species, also mediate pruritus.2-4
This multipart article will explore the common conditions that cause scalp itch and how to treat them in a clinical setting. Part I will address inflammatory dermatologic disorders, and Part II will discuss infectious dermatologic disorders, neuropathic, psychogenic, and systemic disorders.
Figure 1. Patients with psoriasis and scalp pruritus can experience lower work productivity, poor quality of sleep, and decreased emotional health.
Seborrheic Dermatitis
One of the major dermatologic conditions causing scalp itch is SD.4,6 The diagnosis is straightforward with scaling, erythema, and itching as the predominant presenting signs.7,8 About one-third to 50% of the population is affected by SD, which includes dandruff.7,8 The 3 groups that are most affected are infants younger than 3 months, adolescents in puberty, and adults between 40 to 60 years.8 SD should be suspected in immunocompromised patients such as AIDS, malignancies, or organ transplants.8 Patients with Parkinson disease and other neurologic disorders also have a higher prevalence rate.8
The mainstays of treatment are topical anti-inflammatory and antifungal medications (including selenium sulfide, zinc pyrithione, ketoconazole, and ciclopirox).8 Selenium sulfide and zinc can be used as first-line treatment when SD is predominately in the scalp (as dandruff).
Combination therapy with anti-inflammatories or antifungals can boost success rates in tougher cases.9 A recent Cochrane review ascertained that topical anti-inflammatory medications such as mild (class I or II) steroids and calcineurin inhibitors controlled SD.7 Both antifungals and steroids effectively produced short-term clearance, but strong steroids were better than azoles in reducing scaling, erythema, and itching.7 However, another Cochrane review of antifungals for SD found that ketoconazole had 44% lower side effects compared with steroids with both agents having equitable efficacy.10
Topical lithium gluconate, metronidazole, tar, UV-B phototherapy, and systemic antifungals (itraconazole and terbinafine) are also used.8 Systemic therapy is only warranted for disease refractory to topical treatment.8
One small Japanese study on patients affected by SD or psoriasis determined that scalp itch can decrease with appropriate hair-washing methods for more than 12 weeks.11 Detailed information about prewashing, washing with the shampoo (4 weeks of non-antibacterial shampoo, 4 weeks of antibacterial shampoo, and finally 4 weeks of the original non-antibacterial shampoo), rinsing, using conditioner, and drying were provided to the patients.11 At 8 and 12 weeks, there was statistically significant decreases in both scaling and itchiness coupled with decreased amount of total DNA of Malassezia species and bacteria in the scalp.11 Thus, instructing patients to wash hair properly should be an integral component of treatment combined with pharmaceutical therapy.
Psoriasis
Psoriasis is another common dermatologic condition in scalp pruritus.4,12 Itch in psoriasis can be a disconcerting symptom with increased burden due to lower work productivity, poor quality of sleep, and decreased emotional health12,13 (Figure 1). Up to 58% of patients with psoriasis may have scalp itch.12,14 Diagnosis of psoriasis is usually straightforward with characteristic silvery scaling papules and plaques on the body, usually in areas such as the scalp, extensor surfaces, and intergluteal cleft.13 Pruritus of psoriasis is generally cured with treatment of psoriatic lesions, but concomitant treatment of the itch is warranted.15
Mild scalp psoriasis is initially treated with topical vitamin D3 analogs and midpotency topical steroids.16 Moderate to severe disease should be treated with potent corticosteroids with an occlusive formulation, and possibly phototherapy.16 Systemic treatments should be considered for refractory disease.16 Capsaicin 0.025% cream can be used as a treatment for itch, but the face (and genitals) should be avoided.12 Topical treatments such as calcineurin inhibitors, salicylates, pramoxine (anesthetic), and crisaborole (Eucrisa; a topical phosphodiesterase 4 inhibitor) are possible options for itch.12
Currently, systemic therapies, especially biologics, are a major part of psoriasis treatment.12 Systemic therapy for psoriasis is indicated for high-intensity pruritus and for lesions in visible areas such as the scalp.17 Etanercept (Enbrel), ixekizumab (Taltz), ustekinumab (Stelara), and secukinumab (Cosentyx) are biologics with mean reduction of pruritus (using the itch numeric rating scale and visual analog scale) ranging from 3.6 to 5.2.12 A 4-point reduction in the itch numeric rating scale over a period of 12 weeks constitutes a true clinical change.18 Etanercept was the only therapy to fall below this 4-point change. Ixekizumab is possibly the best at reducing itch with an efficacy of 5.2, and significantly better than placebo or etanercept.12,19 The Janus kinase inhibitor tofacitinib (Xelijanz) at 10 mg twice daily reduced itch by 4.8 on the scale.12 Cyclosporin A also led to a decrease in eosinophils in the blood and pruritus in psoriasis.20
Mirtazapine at sub-antidepressant dosages (7.5-15 mg nightly) can treat psoriatic itch, particularly at bedtime.12 The antidepressants, doxepin (10-20 mg 3 times daily) and paroxetine (20 mg daily) are also possible options.15 Gabapentin and pregabalin are also efficacious in treating itch, but data specifically in psoriasis is lacking.12,15 Finally, narrowband UV-B phototherapy has shown efficacy in treating psoriatic scalp lesions and itch.12,15 However, common side effects of phototherapy are burning and itching, so some patients may not find a benefit from this treatment.13,21 Furthermore, hair can act as an obstacle for scalp psoriasis treatment, thus careful exposure and appropriate tools such as a laser hair comb may be necessary.22 Pruritus should be recognized as an important part of the psoriatic clinical picture, and treatment should be tailored to achieve control of both visual and nonvisual symptoms.
Geriatric Xerosis
The geriatric population has an increased propensity to be affected by pruritus.23-26 Data from 4099 patients (age >65 years) in a Turkish hospital over a 5-year period indicated pruritus affected 11.5% of admissions.24 Pruritus incidence increased with age with the group of 65 to 74 years at 10.3%, 75 to 84 years at 14.9%, and older than 85 years at 19.5%.24 Itch is higher in the fall (lower humidity) and lower in the spring (higher humidity).24
A prospective case-control study of geriatric patients with chronic idiopathic generalized pruritus compared with ethnicity and age-matched controls revealed possible differences in skin biophysical properties.23 Affected patients had lower surface sebum content on their forehead and increased baseline transepidermal water loss.23 As individuals age, they lose activity in sebaceous glands, sweat glands, and aquaphorin-3 (an important membrane channel for skin hydration).25,26
Corneodesmolysis is necessary for desquamation to replace older skin cells with newer ones from the basal layer.26 Improper or slowed corneodesmolysis is found in xerotic skin.26 Although a variety of disorders can cause itch in the elderly such as scabies, neurogenic, diabetes, systemic diseases (renal, liver disease, thyroid), hematologic malignancy, pharmaceutical side effects, iron deficiency, and more, we will focus on the most common disorder: xerosis.25 Nonetheless, disorders that can cause xerosis as a secondary factor such as HIV infection, nutritional deficiency, thyroid disease, diabetes, or malignancy should be on the differential.25,26
The geriatric population should eliminate any harsh soaps, detergents, or fabric softeners.25 Warm water should be used for short showers (<10 minutes), and moisturizers should be applied after a shower.25
Ointments especially inhibit evaporation, and offer occlusion and hydration due to elevated lipid content.25 Ammonium lactate 12% lotion and moisturizers act a keratolytic to aid in the corneodesmolysis process.26
Topical corticosteroids can also be useful, but should be used carefully to avoid side effects such as dermal atrophy.25,26 Topical calcineurin inhibitors might be better suited for a prolonged anti-inflammatory effect.25
Atopic Dermatitis
AD can present in the scalp, especially in the pediatric population.27 Although pruritus is a hallmark of AD, it may be hard to delineate in children younger than 2 years.27 Juicy papules, vesicles, and erythema are generally present in the face, trunk, and scalp.27 In 1 study, scaly scalp was seen in about 39% of patients with AD in the first year of life.28 In a study of the inpatient Chinese population with AD, scalp involvement occurred in 70% of infants (<2 years), 14.8% of children (2-12 years), 8.3% of adolescents (12-18 years), and 38.9% of adults (>18 years).29
For a select subset of patients younger than 5 years, avoiding potential trigger factors such as cow’s milk, eggs, wheat, soy, and peanuts is important.27,30 If patients have recalcitrant AD or a consistent history of flare ups after ingestion of a particular food, then food allergy evaluation is warrented.30 High-risk infants can also be bottle-fed partially or extensively hydrolyzed formula, according to the American Academy of Pediatrics.31 For older children and adults, pollen-related foods should be considered as allergic triggers.30 Aeroallergens such as dust mites, dander, and pollen serve as triggers with increasing prevalence as patients grow older.30
Application of moisturizers is paramount in managing AD in both adults and children.32 Moisturizers should be free of additives that may trigger flares such as fragrances and perfumes.32 Use of topical anti-inflammatory agents in infants should be relatively conservative compared with adults due to the higher ratio of body surface: body weight.27,32 Although there is a steroid phobia in parents, and perhaps even in providers, for using topical steroids in children, proper use results in effective and well-tolerated treatment.33,32 Hypothalamic-pituitary-adrenal axis suppression is possible, but rare with topical steroids.33 High-potency topical corticosteroids should be used only in the short term as an induction therapy for controlling disease.33 Moderate potency can be used for the trunk and extremities, and low potency in sensitive areas such as the face, neck, axilla, and genitals.33 The scalp is best treated with foams, solutions, oils, and gels.33 Wet wrap therapy coupled with a topical agent can increase penetration, and serve as a barrier to protect against excoriation.32 Twice-daily application might be necessary for older children and adults, but once daily can be sufficient for young children and infants.32
Topical calcineurin inhibitors are also acceptable for treatment in adults and pediatric populations.32 They can be considered especially in cases recalcitrant to steroids, for sensitive areas (face, neck, genitals), steroid-induced side effects, or combined with long-term use with topical steroids.32 Tacrolimus 0.03% can be used for ages 0 to15 years, and 0.1% for individuals older than 15 years32; twice-daily application is preferred.32 Some providers prefer to use off-label topical calcineurin inhibitors as first-line treatment in patients younger than 2 years.27,32 Maintenance therapy using either topical steroids (1-2 times weekly) or calcineurin inhibitors (2-3 times weekly) can reduce subsequent flare ups.30,32 Patients should be informed of potential cutaneous viral infections and possible malignancy associated with topical calcineurin inhibitors, but the actual risk based on existing data is unclear and probably minimal.32
Article continues on page 2
Bleach baths with intranasal mupirocin demonstrated clinical improvement in treating skin infections associated with AD; however, the clinical improvement was limited to skin submerged in the bath (ie, not the scalp or head).32 Phototherapy can be used to treat AD after failure of the previous treatments or as maintenance therapy.34 Physician-guided phototherapy is preferred to home phototherapy.34 There is no recommendation for a specific type of phototherapy; natural light, narrowband UV-B, broadband UV-B, and topical and systemic psoralen–UV-A are all feasible.34 Dosing should be based on minimal erythema dose and Fitzpatrick skin type.34 Phototherapy can be used as monotherapy or in conjunction with topical steroids.34 However, caution should be exercised with concomitant use with topical calcineurin inhibitors due to manufacturer warning.34 Phototherapy, especially narrowband UV-B, is generally considered safe in the pediatric population.34
If these previous methods fail, systemic therapy with cyclosporine, methotrexate, mycophenolate, and azathioprine can be used.34 However, limited data exists for strong recommendations on dosing, duration, and monitoring in AD.34 Existing general guidelines should be used for preliminary testing, use, monitoring, and adverse effects for systemic immunosuppressants.34 Clinicians must strive to use the lowest possible dosage in both adult and pediatric populations.34 Systemic steroids can be used, but only temporarily to resolve severe flare ups and as a bridge to other systemic therapies.34 Clinical correlation and patient specific treatment is advised.34 Omalizumab (Xolair) is a humanized monoclonal antibody, targeting the Fc receptor of IgE, FDA approved for asthma, and has demonstrated benefit in AD patients.34,35 The newly FDA-approved dupilumab (Dupixent), a humanized monocolonal antibody against IL-4α, has shown strong efficacy in treating moderate to severe AD.36 The most common treatment associated side effects were nasopharyngitis and headache.36 Trials are still ongoing for pediatric populations.36 Structured educational programs for patients and parents can be helpful in reducing disease burden and exacerbations, but require substantial monetary and temporal resources.30
Contact Dermatitis
Contact dermatitis (CD) of the scalp is another source of pruritus. A study of 1320 patch tested patients (for scalp allergic CD) in the Information Network of Departments of Dermatology (IVDK; between 1993 and 2003) revealed hair-coloring agents were the most common allergens causing sensitization.37
The main (commercial patch testing) agents were p-phenylenediamine, tolune-2,5-diamine, p-aminophenol, 3-aminophenol, p-aminoazobenzene, cocamidopropyl betaine, and pyrogallol and caused significantly higher sensitization compared with the remaining IVDK patients.37 Of the study population, 78% were women, but this may be due to over half of all women in industrial nations using hair-coloring substances.37 Patients’ personal products were also tested in 690 patients and revealed that medical products, hair tints, bleaches, and hair-cleansing products caused two-thirds of positive tests in this subgroup.37 Hair tints and bleaches were the most likely culprit, and more than 80% of these patients did not react to an allergen in the commercial patch test.37 Therefore, for a patient who may have allergic CD of the scalp, both commercial patch testing and the patient’s own products is imperative.37Thioglycolate, formaldehyde, lanolin, fragrances, solvents, and surfactants are also possible allergens in cosmetic hair prodcuts.38 Adhesive in hair extension and wigs and topical drugs (such as minoxidil and its the solvent propylene glycol) are possible.39 The chemicals listed are not exhaustive as a variety can trigger an allergic response.39 Affected patients may have pruritus, vesicles, papules, pustules, edema, and erythema on the scalp, but also on the face, neck, and other adjacent areas that the allergen affected.39,40
Irritant CD is also possible with no prerequisite sensitization, and may be more common than its allergic counterpart.38,41 Detergents, shampoo (especially ones with sodium lauryl sulfate), and a variety of entities can cause irritant CD.41 Patients have stinging pain, itching, burning, erythema, and edema.38,40 Although both allergic and irritant CD can cause pruritus, the allergic pruritus is much worse.40 Allergic CD may have more distinct borders and geometrical demarcation, while irritant CD has less distinct borders.40
Treatment for both allergic and CD involves diagnosing the condition and determining the responsible substance.40,41 Cessation and prevention of exposure is the ideal course.40,41 For localized CD, topical mid- to high-potency steroids can offer relief. If sensitive areas (face, eyelids, neck) are included, then a low-potency steroid like desonide should be used.40,41 For CD that involves greater than 20% of the skin or for severe cases, systemic steroid therapy can be prescribed.40,41
Figure 2. Patients with alopecia can experience hair loss and scalp pruritus.
Cicatricial Alopecias
Cicatricial alopecias are a known source of pruritus of the scalp42 (Figure 2). Chronic cutaneous lupus erythematous, especially the form discoid lupus erythematous (DLE) which constitutes 50% to 85% of cases, presents with pruritus, pain, scaling, erythema, and discoloration of the affected scalp.42,43
DLE affects is more prone in women, and cases in African Americans can be more severe.42,43 Limiting sun exposure and wearing sunscreens are part of the preventive treatment.
Topical and intralesional corticosteroids, calcineurin inhibitors, and hydroxychloroquine are the mainstays of treatment.42 Rapidly progressive disease should be treated with hydroxychloroquine first, and slowly progressive disease should be first treated with corticosteroids.43 Oral retinoids are also a possible choice.43 Systemic immunosuppressive therapy may be warranted for severe and generalized disease.42,43
Lichen planopilaris (LPP) and its subtypes classic, frontal fibrosing alopecia (FFA), and Graham Little syndrome are rare cicatricial alopecias.42 LPP usually affects adult women in the crown and parietal areas with generalized or focal areas of disease.42 FFA affects postmenopausal women with a band-like hair loss at the frontal hair line and the eyebrows.42 Graham Little syndrome presents with cicatricial alopecia of the scalp, lichen planus spinulosus, and noncicatricial alopecia of pubic and axillary regions.42 Follicular hyperkeratosis and perilesional erythema are found clinically in all forms of LPP.43 Topical and intralesional steroids are used along with hydroxychloroquine. Cyclosporine and mycophenolate mofetil are used in refractory cases.42 Topical minoxidil can abate further hair loss.42
Central centrifugal cicatricial alopecia is a permanent scarring hair loss predominately affecting African American women. Patients experience pain, burning, and pruritus. The alopecia starts at the vertex and expands symmetrically. As with other cicatricial alopecias anti-inflammatory treatment is first line to reduce progression. Topical and intralesional corticosteroids, topical calcineurin inhibitors, and oral tetracyclines are used. Topical minoxidil is also used promote hair growth.42
Conclusion
Diagnosing the source of scalp pruritus is critical in treating these inflammatory dermatologic disorders. While AD might present with pruritus as one of the most severe symptoms, diseases like psoriasis or cicatricial alopecias might have other symptoms that confound the impact of itching. Dermatologists must be aware and vigilant in treating scalp pruritus.
Mr Subash is a research fellow in the department of dermatology at Wake Forest Baptist Health in Winston-Salem, NC.
Dr McMichael, The Mane Point Section Editor, is professor and chair in the department of dermatology at Wake Forest Baptist Health in Winston-Salem, NC.
Disclosure: Dr McMichael has received grants from Allergan and Proctor & Gamble. She is a consultant for Allergan, eResearch Technology, Inc, Galderma, Guthey Renker, Johnson & Johnson, Keranetics, Merck & Co, Inc, Merz Pharmaceuticals, Proctor & Gamble, Samumed, and Incyte. She receives royalties from Informa Healthcare and UpToDate and also has conducted research for Samumed.
Mr Subash reports no relevant financial relationships.
References
1. Misery L, Rahhali N, Duhamel A, Taieb C. Epidemiology of dandruff, scalp pruritus and associated symptoms. Acta Derm Venereol. 2013;93(1):80-81.
2. Elewski BE. Clinical diagnosis of common scalp disorders. J Investig Dermatol Symp Proc. 2005;10(3):190-193.
3. Grimalt R. A practical guide to scalp disorders. J Investig Dermatol Symp Proc. 2007;12(2):10-14.
4. Bin Saif GA, Ericson ME, Yosipovitch G. The itchy scalp–scratching for an explanation. Exp Dermatol. 2011;20(12):959-968.
5. Reamy BV, Bunt CW, Fletcher S. A diagnostic approach to pruritus. Am Fam Physician. 2011;84(2):195-202.
6. Dall’Oglio F, Lacarrubba F, Verzì AE, Micali G. Noncorticosteroid combination shampoo versus 1% ketoconazole shampoo for the management of mild-to-moderate seborrheic dermatitis of the scalp: results from a randomized, investigator-single-blind trial using clinical and trichoscopic evaluation. Skin Appendage Disord. 2016;1(3):126-130.
7. Kastarinen H, Oksanen T, Okokon EO, et al. Topical anti-inflammatory agents for seborrheic dermatitis of the face or scalp. Cochrane Database Syst Rev. 2014;(5):CD009446. doi:10.1002/14651858.CD009446.pub2
8. Borda LJ, Wikramanayake TC. Seborrheic dermatitis and dandruff: a comprehensive review. J Clin Investig Dermatol. 2015;3(2).
9. Berk T, Scheinfeld N. Seborrheic dermatitis. P T. 2010;35(6):348-352.
10. Okokon EO, Verbeek JH, Ruotsalainen JH, Ojo OA, Bakhoya VN. Topical antifungals for seborrhoeic dermatitis. Cochrane Database Syst Rev. 2015;(5):CD008138. doi:10.1002/14651858.CD008138.pub3
11. Kobayashi M, Ito K, Sugita T, et al. Physiological and microbiological verification of the benefit of hair washing in patients with skin conditions of the scalp. J Cosmet Dermatol. 2016;15(4):e1-e8.
12. Stull C, Grossman S, Yosipovitch G. Current and emerging therapies for itch management in psoriasis. Am J Clin Dermatol. 2016;17(6):617-624.
13. Szepietowski JC, Reich A. Pruritus in psoriasis: An update. Eur J Pain. 2016;20(1):41-46.
14. O’Neill JL, Chan YH, Rapp SR, Yosipovitch G. Differences in itch characteristics between psoriasis and atopic dermatitis patients: results of a web-based questionnaire. Acta Derm Venereol. 2011;91(5):537-540.
15. Reich A, Szepietowski JC. Clinical aspects of itch: psoriasis. In: Carstens E, Akiyama T, eds. Itch: Mechanisms and Treatment. Boca Raton, FL: CRC Press; 2014:chap 4.
16. Ortonne J, Chimenti S, Luger T, Puig L, Reid F, Trüeb RM. Scalp psoriasis: European consensus on grading and treatment algorithm. J Eur Acad Dermatol Venereol. 2009;23(12):1435-1444.
17. Gisondi P, Di Mercurio M, Idolazzi L, Girolomoni G. Concept of remission in chronic plaque psoriasis. J Rheumatol Suppl. 2015;93:57-60.
18. Kimball AB, Naegeli AN, Edson-Heredia E, et al. Psychometric properties of the itch numeric rating scale in patients with moderate-to-severe plaque psoriasis. Br J Dermatol. 2016;175(1):157-162.
19. Kimball AB, Luger T, Gottlieb A, et al. Impact of ixekizumab on psoriasis itch severity and other psoriasis symptoms: results from 3 phase III psoriasis clinical trials. J Am Acad Dermatol. 2016;75(6):1156-1161.
20. Schopf RE, Hultsch T, Lotz J, Bräutigam M. Eosinophils, pruritus and psoriasis: effects of treatment with etretinate or cyclosporin-A. J Eur Acad Dermatol Venereol. 1998;11(3):234-239.
To avoid overdiagnosis, unneeded procedures, and misinformation that can lead to patient stress, we should not refer to clinically atypical moles as being “precancerous."
To avoid overdiagnosis, unneeded procedures, and misinformation that can lead to patient stress, we should not refer to clinically atypical moles as being “precancerous."
Stetson Albertson, DO; Jeffrey Dickman, DO; and Steve Grekin, DO Amor Khachemoune, MD, FAAD, FACMS, Section Editor
An otherwise healthy 56-year-old White woman presented to the dermatology department for evaluation of a rash to the bilateral axillae, wrists, and inframammary folds. What Is The Diagnosis?
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Mr Subash is a research fellow in the department of dermatology at Wake Forest Baptist Health in Winston-Salem, NC.
Mr Subash is a research fellow in the department of dermatology at Wake Forest Baptist Health in Winston-Salem, NC.
