The Effective Management of Hyperkeratosis
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Clinical REVIEW The effective management of hyperkeratosis There are various skin conditions that fall under the umbrella term ‘hyperkeratosis’. and this article looks at the aetiology and subsequent modes of treatment in regards to these conditions. yperkeratosis is an umbrella skin disease of the ichthyosis family, term for a number of skin affecting around 1 in 250,000 people. conditions. It involves a Hthickening of the stratum corneum It involves the clumping of keratin (the outer layer of the skin), often filaments (Freedberg et al, 2003). This 8 Fungal infection associated with a keratin abnormality, is a hereditary disease, the symptoms 8 Hyperkeratosis and is also usually accompanied by an of which are hyperkeratosis, blisters 8 Stratum corneum increase in the granular layer of the and erythema. At birth, the skin of 8 Keratin skin. As the corneum layer normally the individual is entirely covered varies greatly in thickness across with thick, horny, armourlike plates different sites, some experience is that are soon shed, leaving a raw needed to assess minor degrees of surface on which scales then reform. hyperkeratosis (Kumar et al, 2004). Multiple minute digitate This thickening is often the skin’s hyperkeratoses (MMDH) normal protection against rubbing, MMDH is a rare familial or acquired pressure and other forms of irritation, cutaneous eruption of filiform keratosis, causing calluses and corns on the hands typically found across the trunk and and feet or whitish areas inside the extremities. Histopathology, distribution mouth. Other forms of hyperkeratosis and history can distinguish it from occur as part of the skin’s defence other digitate keratoses. Goldstein against chronic inflammation, infection described the first case of MMDH in and the radiation of sunlight or irritating 1967, suggesting the term ‘multiple chemicals. Less often, hyperkeratosis minute digitate hyperkeratosis’ because develops on skin that has not been the projections were numerous, and irritated. These types may be part of an finger-like, comprising a horn of dense inherited condition, may begin soon orthokeratin (Goldstein, 1976). MMDH after birth and can affect skin on large presents with numerous digitate areas of the body (Freedberg et al, 2003). keratoses across the trunk and limbs, with sparing of the face, palms, Types of hyperkeratosis and soles. The keratoses are skin- (hereditary) coloured, rod-shaped, non-follicular, Epidermolytic hyperkeratosis between 1–5mm in length, between This type of hyperkeratosis is 0.3–2mm in diameter, and arise from also known as ‘bullous congenital otherwise normal skin (Caccetta et ANN JAKEMAN is a Tissue Viability ichthyosiform erythroderma’, ‘bullous al, 2010). Nurse at the Royal Brompton and ichthyosiform erythroderma’, or Harefield Foundation Trust, London ‘bullous congenital ichthyosiform Focal acral hyperkeratosis erythroderma Brocq’ and is a rare Also known as ‘acrokeratoelastoidosis Wounds Essentials 2012, Vol 1 65 Clinical REVIEW lichenoides’, this condition is a late-onset condition has been shown in several Seborrheic keratosis keratoderma, inherited as an autosomal small-scale studies to respond well to These are small, non-cancerous skin dominant condition (single parental supplementation with vitamins and growths. They can be tan, brown or gene), characterised by oval or polygonal fats rich in essential fatty acids. Some black and are found on the face, trunk, crateriform papules developing along research suggests this is due mainly arms or legs. These are very common the border of the hands, feet and wrist to vitamins E and B. Vitamin A is and most people develop between one (Freedberg et al, 2003). also thought to be connected to the and 20 during their lifetime. Their cause pathology (Nadiger, 1980). is unknown (Freedberg et al, 2003). Lamellar ichthyosis This is a rare skin condition that Site specific Corns appears at birth and continues Plantar hyperkeratosis A corn is a small area of skin which throughout a person’s life. It is This condition is a circumscribed has become thickened due to the passed down through families and keratotic area which may or may not pressure exerted on it. They are both parents must have at least be associated with a hammered great roughly round in shape and press into one abnormal gene to pass it on toe. Keratosis often resembles verruca the deeper layers of skin, becoming to their children. People with this plantaris, for which it is mistakenly painful. Hard corns commonly occur condition are born with a collodian treated, until the keratosis breaks down on the top of the smaller toes or on membrane — a shiny, waxy layer of and ulcerates or leaves a permanent the outer side of the little toe. These skin that sheds within the first two scar. Although keratosis under the are the areas where poorly fitted weeks of life. Red, scaly skin remains first metatarsal head is common, it is shoes tend to rub the most. Soft corns underneath — this resembles the more usual to have disabling symptoms sometimes form in between the toes, surface of a fish (Morelli, 2007). underneath the middle three metatarsals most commonly between the fourth (Skinner and Fitzpatrick, 2008). and fifth toes. These are softer because X-linked ichthyosis (XLI) the sweat between the toes keeps XLI is also known as ‘steroid sulfatase Hyperkeratosis of the them moist. Soft corns can sometimes deficiency’, as well as ‘X-linked nipple and areola become infected (Freeman, 2002). recessive ichthyosis’ (from the Ancient This is an uncommon benign, Greek ‘ichthys’, meaning ‘fish’) and is a asymptomatic, acquired condition of Calluses skin condition caused by the hereditary unknown pathogenesis. A callus is larger, broader and has a deficiency of the steroid sulfatase (STS) less well-defined edge than a corn. enzyme, affecting between one in 2,000 Lichen planus These tend to form on the underside and one in 6,000 males. XLI manifests Lichen planus may appear as a lacy, of the foot (the sole). They commonly with dry, scaly skin and is due to white patch on the inside of the form over the bony area just deletions or mutations in the STS gene. mouth or as an itchy, violet, scaly underneath the toes. This area takes XLI can also occur in the context of patch elsewhere on the skin. In some much of your weight when you walk. larger deletions, causing contiguous cases, it affects the mouth, genitals, They are usually painless but can gene syndromes. Treatment is largely hair, nails, and rarely, other parts of become painful (Freeman, 2002). aimed at alleviating the skin symptoms the body. About one in 50 people (Gelmetti and Caputo, 2002). develop lichen planus and it occurs Other equally in men and women. More Hyperkeratosis lenticularis Keratosis pilaris than two-thirds of cases occur in perstans (HLP) Also known as ‘follicular keratosis’, people aged 30–60 years, however, Also known as Flegel disease, HLP is keratosis pilaris is a common, it can occur at any age. It is not an a cutaneous condition characterised autosomal dominant, genetic follicular inherited disease, nor is it an infection, by rough, yellow-brown keratotic, condition that is manifested by the and the rash cannot be caught or flat-topped papules of irregular outline appearance of rough bumps on the passed on to others. Although the measuring 1–5mm in diameter and skin. It most often appears on the cause of this condition is unknown, up to 1mm in depth (Rapini et al, back and outer sides of the upper researchers suspect that it may be 2007). Lesions are located primarily on arms (although the lower arms can related to an abnormal reaction of the dorsal feet and lower legs, with a also be affected), and can occur on the immune system. One theory decreasing likelihood of manifestation any body part except glabrous skin is that the immune system may be proximally. Most cases have been (naturally hairless, such as the palms triggered by a virus or other factor in reported in Europe. No instigating factor or soles of the feet). Less commonly, the environment to attack cells in the has been identified clearly, however, lesions appear on the face, which skin, which leads to the inflammation may be mistaken for acne. This (Lehman et al, 2009). Continued on p70 66 Wounds Essentials 2012, Vol 1 Table 1 – Treatment of Hyperkeratosis Type Treatment Side effects Epidermolytic 8 Gene therapy is really the only true therapy 8 Oral retinoid therapy frequently causes revers- hyperkeratososiis for people with EHK. Until gene therapy solu- ible changes in liver function and serum lipid tions finally become a reality, EHK sufferers 8 Up to 75% of retinoid-treated patients experi- must treat their fragile skin carefully. Most ence dose-related hair loss, which is reversible have learned that taking regular, extended upon discontinuation of therapy baths allows patients to care for their fragile 8 Acitretin can cause major foetal abnormali- skin and keep it manageable. Baths that ties and is therefore contraindicated in preg- include sea salt seem to improve the process nant women of softening and removing the thickened skin 8 Topical retinoids are also contraindicated in (Brecher and Orlow, 2003) pregnancy. Local reactions include: burning, 8 Oral retinoids — etretinate, acitretin, erythema, stinging, pruritus, dry/peeling skin isotretinoin (Brecher and Orlow, 2003). Con- (BMJ/RPS, 2012) traindicated in hyperlipidaemia, renal and hepatic impairment 8 Acitretin Multiple minute 8 Topical keratolytics combined with topical 8 Topical keratolytics – can cause pain, itching, digitate emollients burning, irritation, inflammation, dryness, hyperkeratosis 8 Tretinoin cream and oral vitamin A swelling and tenderness at site of application. 8 Topical 5-fluorouracil cream – apply thinly This will heal once treatment is complete to the affected area once or twice per day 8 Tretinoin cream can cause stinging, burning, (max area 500cm2 for three to four weeks dry and peeling skin, sensitivity to UVB light.