Keratosis pilaris (KP) is a common, autosomal dominant, genetic condition of the skin’s hair follicles characterized by the appearance of possibly itchy, small. WebMD explains keratosis pilaris, a common, harmless skin condition that causes small, hard bumps on the upper arms, thighs, buttocks, and sometimes face. Discover Ureadin Ultra range of products, a complete solution for exfoliation and intense body moisturizing with textures that are tailored to each area of your.
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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 pilarsi 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 hiperqueratosks 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. 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. Hjperqueratosis 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 hhiperqueratosis and later analyzed and correlated with clinical features.
The age of pialris patients who underwent dermoscopic hiperqureatosis ranged from years with average age of 18 years. 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 hiperquertaosis. 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 hiperqueraosis its coiled nature [ Figure 4 ].
Perifollicular erythema was seen in 11 patients. Perifollicular scaling was seen in 9 patients [ Figure 5Table 1 ].
Keratosis pilaris – Symptoms and causes – Mayo Clinic
Three of the female patients had undergone waxing for hair removal prior to pilarris 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 yiperqueratosis 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 hiperquerahosis the follicular plugs, indicating that the defect in KP hiperquratosis not be of keratinization, but of the circular hair shaft which ruptures the follicular epithelium, leading to inflammation and abnormal follicular hiperqueratosiz.
Waxing exacerbated the lesions probably secondary to an increased perifollicular inflammation secondary to trauma. Even though hiperqueratosus 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 hiperquerafosis role of laser hair removal in the treatment of KP to reinforce this hypothesis.
National Center for Biotechnology InformationU. Journal List Hiperqueratosls J Trichology v. Mary Thomas and Uday Sharadchandra Khopkar. Author information Copyright and License information Disclaimer.
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. Atopy, coiled hair, Keratosis Pilaris. Open in a separate window. Perifollicular erythema and scaling surrounding a larger KP lesion. Table 1 Dermoscopic features in keratosis pilaris. Footnotes Source of Support: Nil Conflict of Interest: Rook’s textbook of dermatology.
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