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ORIGINAL ARTICLE
Year : 2016  |  Volume : 17  |  Issue : 1  |  Page : 13-17

Juvenile plantar dermatosis: A barrier disease beyond eczema: An open prospective uncontrolled study in a tertiary care hospital of South India


Department of Dermatology, Raja Rajeswari Medical College and Hospital, Kambipura, Bengaluru, Karnataka, India

Date of Web Publication4-Jan-2016

Correspondence Address:
Hari Kishan Kumar
70, Padma Nivasa, Skin Care Clinic, 3rd Cross MG Extension, HV Halli, Rajarajeshwari Nagar, Bengaluru - 560 098, Karnataka
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/2319-7250.173158

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  Abstract 

Background: Juvenile plantar dermatosis (JPD), also known as “wet and dry foot syndrome,” is a skin disorder of the feet that commonly affects children from ages 3–14. JPD is frequently seen in children with eczema, but it is not a requirement for diagnosis. Forefoot eczema (FE) is synonymous with JPD is a condition characterized by dry fissured dermatitis of the plantar surface of the feet.
Aims: To study the clinical patterns of FE and its associated risk factors.
Methods: Twenty-five patients were recorded in the study during the period from April 2013 to March 2014. Fungal scrapings, patch testing, and biopsy for histopathological examination were done wherever required.
Results: In our study, the most common site affected was the plantar surface of the toes in 8 (32%) patients. Hand involvement, with fissuring and soreness of the fingertips and palm, was seen in two patients (8%). Four patients (16%) had a personal history of atopy whereas a family history of atopy was present in 3 (12%). Nine patients (36%) had associated risk factors with reported aggravation of itching with plastic, rubber, or leather footwear, and with prolonged contact with water and detergents. Negative fungal scrapings and culture in all patients ruled out a dermatophyte infection. Patch testing with Indian Standard Series was performed in all patients and was positive in three.
Conclusions: This study concluded FE as a distinctive dermatosis of the first and second decade, predominantly in males, with a multifactorial etiology and confirming the concept of FE as a barrier disease beyond eczema.

Keywords: Barrier disease, eczema, juvenile plantar dermatosis


How to cite this article:
Kumar HK, Naveen S, Shankar K. Juvenile plantar dermatosis: A barrier disease beyond eczema: An open prospective uncontrolled study in a tertiary care hospital of South India. Indian J Paediatr Dermatol 2016;17:13-7

How to cite this URL:
Kumar HK, Naveen S, Shankar K. Juvenile plantar dermatosis: A barrier disease beyond eczema: An open prospective uncontrolled study in a tertiary care hospital of South India. Indian J Paediatr Dermatol [serial online] 2016 [cited 2020 Jul 16];17:13-7. Available from: http://www.ijpd.in/text.asp?2016/17/1/13/173158


  Introduction Top


Forefoot eczema (FE) is a skin condition that generally presents in boys between 3 and 14 years of age, but it may also occur in females. It can also occur in adults of all ages but infrequently when it occurs in children the prognosis is one of gradual improvement. Due to a lack of published data on the condition, its prevalence is not well-known. However, the condition is more common in clinical practice and is poorly understood, whose presentation may mimic that of numerous other common dermatoses. Children's eczema, also known as “juvenile plantar eczema,” has a tendency to be more severe during the summer months.[1],[2] Juvenile plantar dermatosis (JPD) typically presents as an erythematous rash of the weight-bearing plantar aspects of the feet; the distal one-third of the plantar surface of the feet and toes tends to be involved more frequently. The posterior two-thirds of the plantar surface are not involved. Areas of involvement generally appear smooth and shiny with a high incidence of painful fissuring and cracking. Various etiological causes have been postulated for this condition such as an allergic contact dermatitis to footwear, dermatophyte infection, and maceration of the foot following use of occlusive footwear.[1],[3] FE is a clinical diagnosis, although skin scraping to exclude fungus and patch tests to exclude footwear allergy are advised. We conducted a study in our hospital, to look for the clinical profile of patients presenting with FE and its cofactors.


  Methods Top


Twenty-five patients with FE were included in this prospective study during the period from April 2013 to March 2014 after obtaining approval from the Ethics Committee of our institution. The inclusion criteria were erythema, fissuring, and scaling of the soles with or without the involvement of the dorsa of the feet. Patients with well-defined plaques suggestive of psoriasis or with a history suggestive of allergic contact dermatitis were excluded. A detailed history was taken regarding the age of onset, duration of disease, seasonal variation or any aggravating factors, presence of pain or pruritus, personal and family history of atopy, and the areas of the foot affected.

The diagnosis of FE was made primarily on clinical presentation, after excluding dermatophyte infection and allergic contact dermatitis. Dermatophyte infection was ruled out by performing a potassium hydroxide (KOH) mount and culture from the lesions in all patients, and patch testing with the Indian Standard Series (ISS) was performed in those with the involvement of the dorsa of the feet and/or history of aggravation with the use of socks/footwear. Skin biopsies were performed in a few cases for histopathological correlation and to confirm the clinical diagnosis. Histopathologic features included psoriasiform acanthosis, with focal loss of granular cell layer, and uniform parakeratosis. Distinctive features included dermal mononuclear infiltrate to localize around sweat ducts at their point of entry into the epidermis. In addition, spongiosis and occasional spongiotic vesiculation subcorneally, these features were suggestive of subacute to chronic eczema. A thorough analysis was done with all the available clinical data recorded.


  Results Top


Of the 25 patients, 16 (64%) were males and 9 (36%) females with their age ranging from 3 years to 30 years, the youngest child was 3 years old, and the eldest being 30 years [Table 1]. The duration of the disease was 2 years or more in 8 (32%) [Table 2]. Seven (28%) reported deterioration in clinical symptoms during the rainy or winter season and relative improvement during the summer. Nine (36%) complained of pruritus while 6 (24%) had pain due to fissuring.
Table 1: Age at onset of JPD

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Table 2: Duration of JPD

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The most common site to be involved initially was the plantar surface of the great toe and other toes [Figure 1] in 8 (32%), followed by forefoot in 6 (24%), dorsa of the feet in 4 (16%) [Figure 2], intertriginous area in 3 (12%), instep in 1 (4%), and heel in 1 (4%) [Table 3]. Two patients (8%) had involvement of the hands, with fissuring and soreness of the fingertips and palm [Figure 3].
Figure 1: A case of juvenile plantar dermatosis over plantar surface of great toes showing fissuring and scaling

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Figure 2: Erythema, scaling, and fissuring seen over dorsum of the feet

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Table 3: Sites of affection of JPD

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Figure 3: Juvenile plantar dermatosis of the entire feet along with involvement of hands showing fissuring and scaling

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Four patients (16%) gave a personal history of atopy and 3 (12%), a family history. Nine patients (36%) reported aggravation of itching with the use of leather, plastic, or rubber footwear, and with prolonged contact with water and detergents. Patch testing with ISS was performed in 12 patients (48%) who either had involvement of dorsa of the feet and or aggravation with footwear or socks. Patch test was positive in 3 (12%). One patient (4%) showed sensitivity to nickel and two patients (8%) showed sensitivity to gentamicin.


  Discussion Top


Although JPD was first described more than three decades ago,[1],[4] a through literature search showed relatively few publications on the condition. Taken together, information from these few publications suggests that the condition tends to be chronic with an extended course of 2–4 years and that typical interventions may be palliative but not curative.[5],[6]

FE is also known as “JPD,” “forefoot dermatitis,” “atopic winter feet,” “dermatitis plantar is sicca,” “FE,” “peridigital dermatitis,” and “sweating sock dermatitis.”[2]

FE is a skin condition that generally presents in boys from 3–14 years of age, but it may also occur in females. It can also occur infrequently in adults of all ages. JPD typically presents as an erythematous rash of the weight-bearing plantar aspects of the feet; the distal one-third of the plantar surface of the feet and toes tends to be involved more frequently. The postal two-thirds of the plantar surface are not involved. Areas of involvement generally appear smooth and shiny with a high incidence of painful fissuring and cracking. In some cases, the skin of the affected areas desquamates.[1],[5],[7],[8]

The most common site to be involved initially was the plantar surface of the great toe and other toes followed by forefoot, dorsa of the feet, intertriginous area, instep, and heel. The entire sole can be involved in a minority of cases. Few patients can have involvement of the hands, with fissuring and soreness of the fingertips and palm.[1]

Even in our study, the majority of the cases showed the involvement of plantar surface of the toes, followed by forefoot and dorsa of the feet. However, three patients had intertriginous involvement between the first and second web spaces and one each had involvement of instep and heel. Two patients had developed hand eczema. The majority of the patients in our study group, 21 patients belonged to first and second decades, 4 patients were of 21–30 years age group, and two of these adults had hand eczema.

The desquamation of the skin can mimic keratolysis exfoliativa, but this typically presents initially as pin-size white dots that coalesce. Furthermore, keratolysis exfoliativa tends to affect the palms of the hands more often than the feet and is often asymptomatic.[7] The differential diagnosis of JPD also includes tinea pedis. However, tinea pedis typically involves the fourth and fifth toe web spaces, whereas JPD generally spares the toe webs. Although tinea pedis rarely affects small children, clinicians should not assume based on a patient's younger age that a questionable presentation is JPD rather than tinea pedis. A KOH preparation can confirm or rule out tinea.[4],[9] All the patients in our study group showed negative fungal scrapings upon KOH mount and fungal cultures showed no growth.

The exact etiology and pathogenesis of JPD are not well-understood. JPD is often seen in “atopic” children, i.e., those who have atopic dermatitis (AD) (eczema), asthma, or hay fever.[1],[5] Their skin seems generally more sensitive than others. The problem is related to friction. Friction is greater when the foot moves up and down in a shoe, especially when the foot is sweaty.[7] The foot gets wetter in synthetic shoes (e.g., nylon or vinyl) and moves more in open sandals. There is a tendency to be more severe during the summer months when heat and humidity cause the feet to perspire and sweat. The many synthetic materials and chemicals used in the manufacturing process for shoes and socks are a contributing factor in the occurrence of foot eczema. Sweat retention and covering of the feet by woolen or polyester socks aggravates this condition, whereas cotton allows the skin to breathe. Keeping the foot for a long time in a shoe or socks without aeration is an important triggering factor. Changing to leather footwear and wearing cotton socks may help relieve the problem. It is also important that the footwear fits well, and the sole of the foot is not sliding against the insole of the shoe. Walking barefooted on woolen or polyester carpets may contribute to juvenile plantar eczema as this may lead to static electric charges that may play a role in skin dryness and irritation of JPD. It is sometimes difficult to tell JPD apart from AD, contact dermatitis, psoriasis, keratolysis exfoliativa, or a fungal infection. To aid diagnosis, tests such as scrapings and patch tests, may be recommended.[4],[6],[10] The majority of our patients in the study group gave a positive history of aggravation of the lesions during the summer months with hot and humid climates and children using synthetic socks and footwear. All the patients underwent patch testing for possible allergens, and only three showed positivity for nickel and gentamycin.

JPD may be misdiagnosed as classic AD of the foot given the young age of affected individuals. While there is evidence of an association between JPD and AD, they are distinct diagnoses. In a 10-year follow-up of patients diagnosed with JPD, researchers found that 52 percent of JPD patients were atopic and that JPD was often associated with the development of hand eczema in adulthood. About 26% of individuals who had JPD as children experienced hand eczema as adults.[2],[4]

In JPD, when the foot is exposed to moisture over extended periods of time (either through hyperhidrosis or occlusion of the foot via footwear made of nonbreathable synthetic materials), high levels of surface moisture develop. However, it is well-established that exposure to water does not induce skin hydration; in fact, persistent water exposure is shown to disrupt epidermal barrier function.[11],[12] Furthermore, there is recent evidence that transepidermal water loss or increases as temperature increases,[13] a finding that may be relevant because nonbreathable footwear may be associated with higher foot temperatures.

As the disrupted epidermal barrier permits, excessive evaporation of subcutaneous moisture beyond normal evaporation of moisture on the surface of the skin surface water loss, a cycle of further degradation and dysfunction is instigated. With the lack of hydration, desiccated corneocytes on the epidermal layer shrink. It is likely that in the presence of depleted lipids and epidermal proteins, corneocyte adhesion is diminished, and fissures develop.[11],[12],[13]

Another theory posits that in the hot, humid environment of the shoe, sweat becomes “trapped” in the skin, producing corneocyte edema, and exaggerated shearing stress.[3] These observations and findings as in our study data only prove that JPD is a disease involving barrier disruption beyond an eczema.

The treatment Guidelines for JPD are: Reduce friction, wear well-fitting shoes, preferably leather, with cotton socks. Lubricate the dry skin: Greasy moisturisers can be very helpful, including white soft paraffin, particularly applied after a bath and before bed. Dimeticone barrier creams are easier to use during the day, applied every 4 h. Have a rest day: Schedule quiet times with little or no walking to allow the fissures to heal. Cover the cracks: Fissures heal faster when occluded. Topical steroids: Topical steroid ointments are often prescribed for a couple of weeks. If helpful, they should then be reserved for a flare-up, particularly if the affected skin is red or itchy.[1],[2],[5],[7],[8]

There is no specific treatment for JPD. Management strategies include avoidance of excess moisture through the selection of breathable footwear and the avoidance of footwear when possible. This may help to reduce the amount of sweating and also minimizes the effects of occlusion and friction that promote cutaneous peeling and cracking. Topical corticosteroids are frequently used to diminish acute inflammation but do not seem to directly affect the pathogenesis. Therefore, recurrence is common upon discontinuation of corticosteroid therapy. Given that inflammation and barrier dysfunction are primary components of JPD, an anti-inflammatory barrier repair therapy may represent a suitable option for primary or adjunctive treatment in children with the condition. In our study, all the patients were treated with topical mometasone with fusidic acid preparation for 2 weeks, and a urea-containing moisturizer for regular use on both feet along with levocetirizine 5 mg for itching. Upon clearance of the lesions completely, they were advised to continue foot care with dimethicone barrier cream, moisturizers, and avoid ill-fitting footwear which cause friction and perpetuate the disease.


  Conclusions Top


There are few standard treatment options for JPD, a poorly understood and understudied condition. Barrier repair therapies offer a new management option. JPD is a distinctive dermatosis of the first and second decade, predominantly in males, with a multifactorial etiology confirming the concept of FE as a barrier disease beyond eczema. In our clinical experience, twice-daily application of a barrier cream along with moisturizers was associated with significant improvement in the appearance of the foot. Peeling and cracking were significantly reduced, and the patients reported reduced recurrences.

Acknowledgment

Dr. Naveen. S, MS., Vice Dean, Raja Rajeswari Medical College and Hospital immensely for his constant encouragement and logistic support for conducting this study.

Financial Support and Sponsorship

Nil.

Conflicts of Interest

There are no conflicts of interest.

 
  References Top

1.
Brar KJ, Shenoi SD, Balachandran C, Mehta VR. Clinical profile of forefoot eczema: A study of 42 cases. Indian J Dermatol Venereol Leprol 2005;71:179-81.  Back to cited text no. 1
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van Diggelen MW, van Dijk E, Hausman R. The enigma of juvenile plantar dermatosis. Am J Dermatopathol 1986;8:336-40.  Back to cited text no. 2
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Cravello B, Ferri A. Relationships between skin properties and environmental parameters. Skin Res Technol 2008;14:180-6.  Back to cited text no. 3
    
4.
Ashton RE, Griffiths WA. Juvenile plantar dermatosis – Atopy or footwear? Clin Exp Dermatol 1986;11:529-34.  Back to cited text no. 4
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Svensson A. Prognosis and atopic background of juvenile plantar dermatosis and gluteo-femoral eczema. Acta Derm Venereol 1988;68:336-40.  Back to cited text no. 5
    
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Moorthy TT, Rajan VS. Juvenile plantar dermatosis in Singapore. Int J Dermatol 1984;23:476-9.  Back to cited text no. 6
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Gibbs NF. Juvenile plantar dermatosis. Can sweat cause foot rash and peeling? Postgrad Med 2004;115:73-5.  Back to cited text no. 7
    
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Kalia S, Adams SP. Dermacase. Juvenile plantar dermatosis. Can Fam Physician 2005;51:1203, 1213.  Back to cited text no. 8
    
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Broberg A, Faergemann J. Scaly lesions on the feet in children – Tinea or eczema? Acta Paediatr Scand 1990;79:349-51.  Back to cited text no. 9
    
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Stables GI, Forsyth A, Lever RS. Patch testing in children. Contact Dermatitis 1996;34:341-4.  Back to cited text no. 10
    
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Harding CR. The stratum corneum: Structure and function in health and disease. Dermatol Ther 2004;17 Suppl 1:6-15.  Back to cited text no. 11
    
12.
Elias PM, Choi EH. Interactions among stratum corneum defensive functions. Exp Dermatol 2005;14:719-26.  Back to cited text no. 12
    
13.
Meyer-Hoffert U. Reddish, scaly, and itchy: How proteases and their inhibitors contribute to inflammatory skin diseases. Arch Immunol Ther Exp (Warsz) 2009;57:345-54.  Back to cited text no. 13
    


    Figures

  [Figure 1], [Figure 2], [Figure 3]
 
 
    Tables

  [Table 1], [Table 2], [Table 3]



 

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