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Keratosis pilaris KP is characterized by keratinous plugs in the follicular orifices and varying degrees of perifollicular erythema. The most accepted theory of its pathogenesis proposes defective keratinization of the follicular epithelium resulting in a keratotic infundibular plug. We decided to test this hypothesis by doing dermoscopy of patients diagnosed clinically as keratosis pilaris. Patients with a clinical diagnosis of KP seen between September and December were included in the study.
A clinical history was obtained and examination and dermoscopic evaluation were performed on the lesions of KP. The age of the patients ranged from years. Sixteen patients had history of atopy.
Nine had concomitant ichthyosis vulgaris. All the 25 patients were found to have coiled hair shafts within the affected follicular infundibula. The hair shafts were extracted with the help of a sterile needle and were found to retain their coiled nature. Perifollicular erythema was seen in 11 patients; perifollicular scaling in 9. Based on our observations and previously documented histological data of KP, we infer that KP may not be a disorder of keratinization, but caused by the circular hair shaft which ruptures the follicular epithelium leading to inflammation and abnormal follicular keratinization.
Keratosis pilaris KP is an autosomal dominant disorder that is classically characterized by keratinous plugs in the follicular orifices and varying degrees of perifollicular erythema [ Figure 1 ].
In general, KP is frequently cosmetically displeasing but medically harmless. Keratosis pilaris: Keratotic follicular papules present on the extensor aspect of both forearms. These include phrynoderma, follicular eczema, follicular lichen planus, juvenile pityriasis rubra pilaris, acne vulgaris, acneiform drug eruption, trichostasis spinulosa, ichthyosis follicularis, scurvy, eruptive vellus hair cysts and perforating folliculitis.
The pathogenesis of KP is still not well understood. The most accepted theory proposes defective keratinization of the follicular epithelium resulting in a keratotic infundibular plug. We correlated the findings with the clinical features in these cases to further our understanding of the disease. A cross-sectional, observational study was conducted on 25 patients who presented to our outpatient department between September and December and were clinically diagnosed with KP.
A clinical history was obtained; examination and dermoscopic evaluation were performed on the lesions of KP. Still images of the lesions were shot and later analyzed and correlated with clinical features.
The age of the patients who underwent dermoscopic examination ranged from years with average age of 18 years. The male:female ratio was Of the 25 patients included in the study, 16 patients had history suggestive of atopy. Nine patients had concomitant ichthyosis vulgaris. One other patient had concomitant follicular eczema.
All the 25 patients were found to have circular, twisted or coiled hair shafts within the affected follicular infundibula which could be extracted using a 26G needle. Six patients were found to have small papules of keratosis pilaris; 19 had larger lesions. Dermoscopic examination with white light revealed that all the small papules of KP had a coiled or semicircular intermediate hair embedded superficially in the epidermis.
None of the small lesions had perifollicular erythema or perifollicular scaling [ Figure 2 ]. In larger lesions, a coiled hair shaft was visualized emerging from the infundibulum. The hair shaft formed a semicircle in 3 patients and a loop in 5 patients [ Figure 3 ]. Even after the coiled hair shaft, embedded in the uppermost epidermis was dislodged from it with the help of a needle, it continued to maintain its coiled nature [ Figure 4 ]. Perifollicular erythema was seen in 11 patients.
Perifollicular scaling was seen in 9 patients [ Figure 5 , Table 1 ]. Three of the female patients had undergone waxing for hair removal prior to the dermoscopic evaluation but coiled hair could be visualized embedded in the superficial epidermis even in these cases. It was noted that perifollicular erythema was more prominent in these cases.
Early KP lesion with a circular hair shaft emerging from a normal-appearing follicular opening. A looped hair shaft a and a coiled hair shaft b associated erythema and pigmentation.
Note lack of keratin plug in a. The hair shaft retains its coiled nature even after being extracted from the superficial epidermis with a sterile needle.
Keratosis pilaris is believed to be a disorder of keratinization[ 13 ] and there is very limited literature describing its etiopathogenesis. There are no previous studies evaluating the dermoscopic features of KP.
It is proposed to be a disorder of the keratinocytes caused by a mutation in the FLG gene which codes for fillagrin that is responsible for inducing both hyperkeratosis and inflammatory changes. More than 22 mutations have been described till date. It has also been suggested that insulin resistance may play a role in the development of keratosis pilaris. Currently available treatment modalities for KP include various keratolytics, vitamin D3 analogs, topical systemic retinoids and various laser therapies.
This prompted us to evaluate the clinical and dermoscopic features of KP and review the etiological hypotheses. Upon dermoscopy, we consistently found circular hair shafts mostly within normal-appearing follicular openings.
White light examination revealed the clinically visible follicular papules harboring a circular hair shaft embedded in their sides, but sans follicular plugs. At times, these papules showed the hair to be thicker and forming larger coils embedded in the superficial epidermis. These hair shafts were found to retain their coiled nature even after they were extracted from the follicular plugs, indicating that the defect in KP may not be of keratinization, but of the circular hair shaft which ruptures the follicular epithelium, leading to inflammation and abnormal follicular keratinization.
Waxing exacerbated the lesions probably secondary to an increased perifollicular inflammation secondary to trauma. Even though keratosis pilaris is a common clinical diagnosis, little is known about its etiology.
It was considered to be a defect in the follicular keratinization, though dermoscopic examination did not support this theory. We propose that KP is primarily caused by a hair shaft defect. Further studies are required to evaluate the role of laser hair removal in the treatment of KP to reinforce this hypothesis. Source of Support: Nil. Conflict of Interest: None declared.
National Center for Biotechnology Information , U. Journal List Int J Trichology v. Int J Trichology. Mary Thomas and Uday Sharadchandra Khopkar. Author information Copyright and License information Disclaimer. Address for correspondence: Dr. E-mail: moc. This is an open-access article distributed under the terms of the Creative Commons Attribution-Noncommercial-Share Alike 3. This article has been cited by other articles in PMC. Abstract Background: Keratosis pilaris KP is characterized by keratinous plugs in the follicular orifices and varying degrees of perifollicular erythema.
Materials and Methods: Patients with a clinical diagnosis of KP seen between September and December were included in the study. Results: The age of the patients ranged from years. Conclusion: Based on our observations and previously documented histological data of KP, we infer that KP may not be a disorder of keratinization, but caused by the circular hair shaft which ruptures the follicular epithelium leading to inflammation and abnormal follicular keratinization.
Keywords: Atopy, coiled hair, Keratosis Pilaris. Open in a separate window. Figure 1. Figure 2. Figure 3. Figure 4. Figure 5. Perifollicular erythema and scaling surrounding a larger KP lesion. Table 1 Dermoscopic features in keratosis pilaris. Alai NN. Keratosis pilaris. Disorders of keratinization. Rook's textbook of dermatology.
Oxford, England: Blackwell Publishing; Rogers M. Keratosis pilaris and other inflammatory follicular keratotic syndromes. Fitzpatrick's dermatology in general medicine.
New York: McGraw Hill; Textbook of dermatology. Oxford Blackwell Scientific Publication; The prevalence of accentuated palmoplantar markings and keratosis pilaris in atopic dermatitis, autosomal dominant ichthyosis and control dermatological patients. Br J Dermatol. Cicatricial Alopecia and Keratosis Pilaris. Keratosis follicularis spinulosa decalvans. Arch Dermatol. Cutaneous presentation of the cardio-facio-cutaneous syndrome.
Keratosis pilaris KP also follicular keratosis , lichen pilaris , or colloquially chicken skin  is a common, autosomal dominant , genetic condition of the skin's hair follicles characterized by the appearance of possibly itchy , small, gooseflesh -like bumps, with varying degrees of reddening or inflammation. There are several types of keratosis pilaris and it has been associated with pregnancy , type 1 diabetes mellitus , obesity , dry skin , allergic diseases e. The cause of keratosis pilaris is incompletely understood. As of , keratosis pilaris is thought to be due to abnormalities in the process of depositing the protein keratin in hair follicles, abnormalities in the hair shaft, or both. Keratosis pilaris is the most common disorder of the hair follicle in children.
Keratosis Pilaris Revisited: Is It More Than Just a Follicular Keratosis?
Keratosis pilaris causes small bumps to appear on the upper arms, legs or buttocks. They usually don't hurt or itch. Keratosis pilaris ker-uh-TOE-sis pih-LAIR-is is a common, harmless skin condition that causes dry, rough patches and tiny bumps, usually on the upper arms, thighs, cheeks or buttocks. The bumps generally don't hurt or itch.
Keratosis pilaris: Diagnosis and treatment
DermNet provides Google Translate, a free machine translation service. Note that this may not provide an exact translation in all languages. Keratosis pilaris is a very common form of dry skin characterised by hair follicles plugged by scale. Keratosis pilaris Keratosis pilaris rubra. Keratosis pilaris affects up to half of normal children and up to three-quarters of children with ichthyosis vulgaris a dry skin condition due to filaggrin gene mutations. It is also common in children with atopic eczema. Although most prominent during teenage years, and least common in the elderly, it may occur in children and adults of all ages.