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What is Keratosis Pilaris?

Question:

Discuss about the Keratosis Pilaris.

Keratosis pilaris is a common benign skin disorder. The condition is characterized by the appearance of sometimes itchy, tiny, goose bump like eruptions on the skin that sometimes occur with inflammation .Gerbig, A. W,(2012) indicates that on most occasions the eruptions appear on the lateral aspect of the upper arm,face,trunk and the surface of the gluteus region. The appearance of Keratosis pilaris is uncommon on glabrous skin. This skin abnormality results in spotting of the skin accompanied by irritation hence a scratching reflex. The scratching results in inflammation, worsened by cold environment and pregnancy. Keratosis pilaris is also common in the pediatric population especially in children with ichthyosis vulgaris and atopic eczema (B. Mevorah, A. Marazzi, E. Frenk,2015). The occurrence in the aged population is variable but with the elderly it is uncommon.

The condition is caused by abnormal distribution of keratin lining the proximal portion of the follicular infundibulum. This ends up in scale filling of the follicle limiting physiological exfoliation. Genetic inheritance also determines the manifestation (Gerbig, A. W., 2012). The trait is autosomal dorminant hence with exposure the penetrance in next generation has an increased incidence of having the condition. Dermal distribution of Keratosis pilaris(KP) is quite symmetrical and scaly spots appear red or brown and may not be sore. The clinical expression is also determined by both environmental condition and humidity. There is strong association between FLG mutations and Keratosis Pilaris cold regions than equatorial locales (S.C. Cai et Al, 2012).There is also evidenced increase acquired cases of KP in underlying diseases like diabetes, obesity and Vitamin A deficiency malnutrition.

KP has an unknown pathogenesis. It is based on hyperkeratinization of the skin. There is a crucial association between KP and atopic dermatitis thus a possibility of association of KP with the FLG deficiency. The FLG protein is a major structural protein of the dermis which aggregates keratin filaments to corneocytes and is also hydrolyzed to individual amino acids with osmotically active properties (S. Kezic et al, 2011) . The amino acids contribute to 50% of the moisturization of the stratum corneum and also facilitate photo protection and acidification of the skin surface. The study done by (Khumalo et al.., 2012) indicates nonsense mutations of the FLG protein end up in reduction of stratum corneum moisturization. More to this, the hair is trapped beneath the keratin debris. Erythema occurs around the hair follicles because of local inflammation. The coiled hair is visible beneath the papule, the papules being a result of accumulation of keratin all around the follicular orifice limiting hydration, sweating and excretion.

KP affects the functioning of the skin and the clinical manifestation is a nuisance. The itch, skin dryness and the inflammation on skin is uncomfortable. Management involves resurfacing procedures which can be chemical or microdermabrasion (Klar et al, 2015 ).Microdermabrasion techniques involve use of a microcrystal spray on the stratum corneum to remove excess keratin. There is regeneration of the stratum corneum with increased synthesis of collagen and elastin filaments on the dermal surface. This procedure is suitable for minute and superficial scars and procedures reliable outcomes on skin papules. In some instances the procedure can aggravate acne and result in an hypersensitivity reaction worsening the prognosis especially in individuals with autoimmune disorders and diabetes. Chemical methods unlike mcrodermabrassion are suitable of deep scars and active cases of acne. Various combinations of dermal ointments containing glycolic acid, lactic acid, retinol, urea or salicylic acid are used. The application of chemical or peel ointments including alfa-hydroxy acids (AHA) are productive after skin exfoliation and produce better accuracy with an increased surface area of skin covered (Fischer et al,2010).

Causes of Keratosis Pilaris

The specificity of a resurfacing procedure is determined by the patients’ allergic response and the state of the dermis. In cases of erythema around affected regions, application of chemical peels is suitable. Inflammation requires the application of steroids including predisilone to manage the local inflammation. Microdermabrassion on the other hand is an independent procedure. The procedure involves direction of a stream of micro-aluminum oxide crystals to the affected dirt. A gun is placed on the individual skin at a constant emission rate and duration. The crystals from the gun exfoliate the stratum corneum and the affected hyperkeratinized papules. The mild suction produced results on the removal of the skin debris and the remaining tiny aluminum crystals.

Furthermore, removal of the excess hyperkeratinized skin facilitates regeneration of the stratum corneum from the underlying dermal epithelium .The body response mechanism triggers synthesis of new collagen and elastin filaments reinforced with keratin. Skin therapy by the procedure produces thick and healthy strata. Treatment involve multiple sessions for a better outcome with a common reference of six to ten sessions on a programmed span break of two weeks between sessions under the patients specification module and response to treatment. Microdermapression is usually painless and a single session takes half an hour to a full hour under sterile conditions. Treatment of KP using the set procedure causes exfoliation and synthesis of skin and increased sensitivity to stimuli and light that should be managed.

The skin is covered with Keratin which forms the barrier to physical, mechanical and chemical modalities that may result in injury. There is also protection from the entry of bacteria that would end up causing an infection .Microdermabrassion results in the exfoliation this external surface and limits the protection mechanism. The pilosebaceous unit is also responsible for the protection through the production of secretions including sweat that provide the chemical barrier. The resurfacing procedure results in the removal of most of the protective layer due to the peeling process of the hyperkeratinized skin. Initiation of the healing process involves the stem cells in the stratum basale, which has regenerative capacity.

Stratum corneum replacement involves a physiological feedback mechanism, the stratum corneum work in homeostasis with the underlying stratum basale. The process of desquamation skin cells off the skin occurs in tandem with the proliferation of the new keratinocyctes formed in the germinative layer, the stratum Basale (Hwang, S., & Schwartz, R. A…, 2008). After the procedure of microdermapression, most of the stratum corneum is exfoliated, the process of cornificartion ensues. Cornification involves the transformation of the living keratinocytes within the stratum germinativum into dead corneocytes .The cell membrane of the keratinocytes is replaced with a layer of complexes ceramides that are covalently linked to the structural proteins of the stratum corneum (Imokawa et al, (2011)). The interlinking between elements results in creation of a new barrier. Corneodesmosomes are also form the adhesive junction providing the link to the epidermis. Proteases also degrade the zona adheherens these cells are shed to the dermal surface. The formation and resultant desquamation of the stratum corneum maintains the nature of the skin (Van Smeden et al,(2014)   )

Symptoms of Keratosis Pilaris

Keratinization is a crucial process in the regeneration of the skin after treatment and considering keratin as the major cause of KP the process is allowed to occur at a controlled process (S. J. Chapman,2015 ). Keratin is a complex protein and it allows for skin hydration and the glossy appearance of the skin. The stratum lucidum allows for the concentrating of keratin and making the keratin tough before the keratin is taken up the epidermis to the skin surface in the surfaces of the skin subjected to more friction. The stratum corneum keratinization after microdermabrssion takes into account of the possibility of hyperkeratinization hence the review of the sessions. The normal thickness after regeneration is from 15 to 40μm (Matsui, T., & Amagai, M. (2015)). 

Treatment of Keratosis pilaris is taken form various approaches. The significant surface techniques involve surface microdermapression, the chemical peel technique and the application of fractional laser treatment regimen dependent on fractional laser therapy is a dynamic approach taken up in the last decade. The process involves a fractional carbon (iv) oxide laser therapy using 10,600 nm eCO2 laser. Lee et al (2013) argues that pulse energy from the laser was set at 24-30 mJ and a spot density of 300 spots/cm2 in a static mode.2 passes are delivered using a 300-density tip. The pain is minimized by the application of a local anesthetic cream and applied under occlusion for 30 minutes prior to the initiation of the laser treatment procedure. An air cooling device is also set and cold air at a cooling level of 4used in the laser therapy. The therapy is repeated after three weeks and follow up done to the 12th week.

Microdermabrassion treatment involves removal of the superficial dermis thus re-epithelization occurs. In standard procedures, a wire brush or a fraise with diamond chip are used to abrade the skin whereas in some instances laser dermabrassion where an argon laser is used. In the typical microdermabrasion, a vacuum device with a jet of aluminum oxide crystals is set between 20-40 KpA and used on affected skin (Gerbig, A. W.2012) ). The hand piece is set to a constant flow are and directed towards the skin surface. The machine abrasion created by the flow of the crystals and suction remove the damaged portion of the dermis. The crystal polish the skin surface and increase blood flow the site of abrasion thus triggers the formation of collagen. The procedure is set for up to 30 minutes and no anesthesia is used. The procedure is contraindicated in patients with an acne vulgaris for which chemical treatment is suited (Hwang, S., & Schwartz, R. A, (2008).Chemical peeling techniques are also applied to remove the excess keratin and damaged skin. Application of the peel removes the layers of keratin and stimulates the growth of new skin tissue (Van Smeden,2014 ) The peels may be superficial, medium or deep. Superficial peels use glycolic acid and salicylic acid (Strauss et al, 2012). The components ( 2-3% salicylic acid in urea cream ) are applied on the skin surface and reduce the pigmentation and dryness; recurrent peels lead to better outcomes. In the deep peels, Trichloroacetic acid is used on a concentration of 15-25%, the application once made the peeling is done. This procedure is painful and result in swelling. Deep peels involve application of phenol; this requires monitoring of toxicity and the heart rate. Pre-treatment creams in the form of glycolic acid and hyroxyquinone are applied. Peeling is done after the area is cleaned, chemical applied and treatments of suspected condition made

Treatment Options for Keratosis Pilaris

Microdermapression is a vital treatment avenue in Keratosis pilaris. Execution of the procedure according to protocol ensures quick results. The recovery of the skin from the procedure is immediate since there is minimal invasion. Treatment sessions in KP undertaken on regular intervals results in improvement in the skin hydration, the skin color, tone and aeration of the pilosebaceous unit. Effectiveness of the therapy is also dependent of the preparation techniques. Adverse reaction after sessions include increased predisposition to sun burns and infections if not properly executed

Laser treatment of KP has a high index of positive outcome. In Keratotic papules, there is an indicated grade 2 improvement from the treatment after a 4 week follow up. In the same case, there was a grade 3 improvement in a follow up after 12 weeks thus an indication of better prognosis with increased healing time. Hyperpigmentation a similar indication and reduction in the number of lesions from the condition observed with an increased healing time and longer follow up span ( S. Kezic,2014). Matsui, T., & Amagai..,2015 elucidate that erythema after the laser therapy was of minimal note and there is a minimal likelihood of complications from the condition. Laser treatment has an indication of pain and burning sensation and hypo pigmentation has been indicated in some cases after therapy.

Peeling is a straightforward technique with medium efficacy, after the procedure, mild dermal rubra occurs which resolves within 48 hours. There is minimal effect to the daily individual routine. In the moderately deep peels, the chemical applied may trigger immune response thus localized inflammation occurs (L. Poskitt and J. D. Wilkinson,1994 ). The inflammation is managed by Non Steroidal Antinflammmatory drugs and resolves in 7 days. Deeper peels require care, moisturization, cooling and minimal exposure to light for up to six months. Positive outcomes are more common although infections from Staphylococcus aureus, comdones and blotchy skin pigmentation may occur. Combination therapy is commonly used for better outcomes.

In conclusion, it is clear that surface technique produce good prognosis in the management of Keratosis pilaris.

References

Mevorah, A. Marazzi, E. Frenk. (2015).The prevalence of accentuated palmoplantar markings and keratosis pilaris in atopic dermatitis, autosomal dominant ichthyosis and control dermatological patients Br J Dermatol, 112 pp. 679-685

Bukhari, I. A., Al Ghamdi, N., Al Zahrani, A., & Al Shawarby, M. (2015). Generalized keratosis pilaris rubra. Our Dermatology Online, 6(2), 187-189.

Fischer, T. C., Perosino, E., Poli, F., Viera, M. S., & Dreno, B. (2010). Chemical peels in aesthetic dermatology: an update 2009. Journal of the European Academy of Dermatology and Venereology, 24(3), 281-292.

Garg T, Chander R, Jain A. (2011) Combination of microdermabrasion and 5-fluorouracil to induce repigmentation in vitiligo: An observational study. Dermatol Surg.;37(12):1763-766

Gerbig, A. W. (2012). Treating keratosis pilaris. Journal of the American Academy of Dermatology, 47(3), 457.

Gruber, R., Sugarman, J. L., Crumrine, D., Hupe, M., Mauro, T. M., Mauldin, E. A., ... & Elias, P. M. (2015). Sebaceous gland, hair shaft, and epidermal barrier abnormalities in keratosis pilaris with and without filaggrin deficiency. The American Journal of Pathology, 185(4), 1012-1021.

Hwang, S., & Schwartz, R. A. (2008). Keratosis pilaris: a common follicular hyperkeratosis. Cutis, 82(3), 177-180.

Imokawa, G., Abe, A., Jin, K., Higaki, Y., Kawashima, M., & Hidano, A. (2011). Decreased level of ceramides in stratum corneum of atopic dermatitis: an etiologic factor in atopic dry skin?. Journal of Investigative Dermatology, 96(4), 523-526

Khumalo, N. P., Loo, W. J., Hollowood, K., Salvary, I., Graham, R. M., & Dawber, R. P. R. (2012). Keratosis pilaris atrophicans in mother and daughter. Journal of the European Academy of Dermatology and Venereology, 16(4), 397-400.

Klar, J., Schuster, J., Khan, T. N., Jameel, M., Mäbert, K., Forsberg, L., ... & Dahl, N. (2015). Whole exome sequencing identifies LRP1 as a pathogenic gene in autosomal recessive keratosis pilaris atrophicans. Journal of medical genetics, 52(9), 599-606.

Lee, S. J., Choi, M. J., Zheng, Z., Chung, W. S., Kim, Y. K., & Cho, S. B. (2013). Combination of 595-nm pulsed dye laser, long-pulsed 755-nm alexandrite laser, and microdermabrasion treatment for keratosis pilaris: retrospective analysis of 26 Korean patients. Journal of Cosmetic and Laser Therapy, 15(3), 150-154.

Poskitt and J. D. Wilkinson.( 1994 )“Natural history of keratosis pilaris,” British Journal of Dermatology, vol. 130, no. 6, pp. 711–713,.

Matsui, T., & Amagai, M. (2015). Dissecting the formation, structure and barrier function of the stratum  corneum. International immunology, 27(6), 269-280.

Okouchi, M., Kubo, A., Kawasaki, H., Yoshida, K., Ishii, K., Furuse, M., & Amagai, M. (2015). Epidermal tight junction barrier function is altered by skin inflammation, but not by filaggrin-deficient stratum corneum. Journal of dermatological science, 77(1), 28-36.

Paller, A. S., & Mancini, A. J. (2015). Hurwitz Clinical Pediatric Dermatology E-Book: A Textbook of Skin Disorders of Childhood and Adolescence. Elsevier Health Sciences.

Poskitt, L., & Wilkinson, J. D. (2013). Natural history of keratosis pilaris. British Journal of Dermatology, 130(6), 711-713.

J. Chapman, A. Walsh, S. M. Jackson, and P. S. Friedmann.(2012).“Lipids, proteins and corneocyte adhesion,” Archives of Dermatological Research, vol. 283, no. 3, pp. 167–173.

Kezic, G.M. O'Regan, N. Yau, A.Sandilands, H. Chen, L.E. Campbell, K.Kroboth, R. Watson, M. Rowland, W.H.McLean, A.D. Irvine.( (2011),)“Levels of filaggrin degradation products are influenced by both filaggrin genotype and atopic dermatitis severity’’Allergy,  66 pp. 934-940 

Strauss JS, Krowchuk DP, Leyden JJ, et al. American Academy of Dermatology. Guidelines of care for acne vulgaris management. J Am Acad Dermatol.(2007);56-651-653.Available at https://www.aad.org/NR/rdonlyres/8D4D2DDB-7176-4202-808E28D67334B3E4/0/AcneVulgaris.pdf. Accessed December 18, 2012.

Van Smeden, J., Janssens, M., Gooris, G. S., & Bouwstra, J. A. (2014). The important role of stratum corneum lipids for the cutaneous barrier function. Biochimica et Biophysica Acta (BBA)-Molecular and Cell Biology of Lipids, 1841(3), 295-313.

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