Clinical Dermatology - part 3 pot

66 CHAPTER 6 cillamine. Contact with chemicals used to develop colour film can also produce similar lesions. It may be hard to tell lichen planus from generalized dis- coid lupus erythematosus if only a few large lesions are present, or if the eruption is on the palms, soles or scalp. Wickham’s striae or oral lesions favour the diagnosis of lichen planus. Oral candidiasis (p. 000) can also cause confusion. Investigations The diagnosis is usually obvious clinically. The his- tology is characteristic (Fig. 6.7), so a biopsy will confirm the diagnosis if necessary. Treatment Treatment can be difficult. If drugs are suspected as the cause, they should be stopped and unrelated ones sub- stituted. Potent topical steroids will sometimes relieve symptoms and flatten the plaques. Systemic steroid courses work too, but are recommended only in special situations (e.g. unusually extensive involvement, nail destruction or painful and erosive oral lichen planus). Treatment with photochemotherapy with psoralen and ultraviolet A (PUVA; p. 59) or with narrow-band UVB (p. 58) may reduce pruritus and help to clear up the skin lesions. Acitretin (Formulary 2, p. 349) has also helped some patients with stubborn lichen planus. Antihistamines may blunt the itch. Mucous membrane lesions are usually asymptomatic and do not require treatment; if they do, then applications of a corticosteroid or tacrolimus in a gel base may be helpful. fine longitudinal grooves to destruction of the entire nail fold and bed (see Fig. 13.26). Scalp lesions can cause a patchy scarring alopecia. Course Individual lesions may last for many months and the eruption as a whole tends to last about 1 year. How- ever, the hypertrophic variant of the disease, with thick warty lesions usually around the ankles (Fig. 6.6), often lasts for many years. As lesions resolve, they become darker, flatter and leave discrete brown or grey macules. About one in six patients will have a recurrence. Complications Nail and hair loss can be permanent. The ulcerat- ive form of lichen planus in the mouth may lead to squamous cell carcinoma. Ulceration, usually over bony prominences, may be disabling, especially if it is on the soles. Any association with liver disease is probably caused by the coexisting hepatitis infections mentioned above. Differential diagnosis Lichen planus should be differentiated from the other papulosquamous diseases listed in Table 6.1. Lichenoid drug reactions can mimic lichen planus closely. Gold and other heavy metals have often been implicated. Other drug causes include antimalarials, β blockers, non-steroidal anti-inflammatory drugs, para-aminobenzoic acid, thiazide diuretics and peni- Hyperkeratosis Prominent granular layer Basal cell degeneration Sawtooth dermo- epidermal junction Colloid bodies Band-like upper dermal lymphocytic infiltrate Fig. 6.7 Histology of lichen planus. CD3C06 21/5/05 11:50 AM Page 66 PAPULOSQUAMOUS DISORDERS 67 Differential diagnosis Psoriasis is the disorder closest in appearance to pity- riasis rubra pilaris, but lacks its slightly orange tinge. The thickening of the palms and soles, the follicular erythema in islands of uninvolved skin, and follicular plugging within the plaques, especially over the knuck- les, are other features that help to separate them. Investigations A biopsy may help to distinguish psoriasis from pityriasis rubra pilaris; but, even so, the two disorders share many histological features. Treatment The disorder responds slowly to systemic retinoids such as acitretin (in adults, 25–50 mg/day for 6–8 months; p. 349). Oral methotrexate in low doses, once a week may also help (p. 348). Topical steroids and kerato- lytics (e.g. 2% salicylic acid in soft white paraffin) reduce inflammation and scaling, but usually do not suppress the disorder completely. Systemic steroids are not indicated. Parapsoriasis and premycotic eruption Parapsoriasis is a contentious term, which many would like to drop. We still find it useful clinically for lesions that look a little like psoriasis but which scale subtly Pityriasis rubra pilaris Cause Several types have been described, but their causes are unknown. A defect in vitamin A metabolism was once suggested but has been disproved. The familial type has an autosomal dominant inheritance. Presentation The familial type develops gradually in childhood and persists throughout life. The more common acquired type begins in adult life with redness and scaling of the face and scalp. Later, red or pink areas grow quickly and merge, so that patients with pityriasis rubra pilaris are often erythrodermic. Small islands of skin may be ‘spared’ from this general erythema, but even here the follicles may be red and plugged with keratin (Fig. 6.8). Similarly, the generalized plaques, although otherwise rather like psoriasis, may also show follicular plugging. Course The palms and soles become thick, smooth and yellow. They often fissure rather than bend. The acquired form of pityriasis rubra pilaris generally lasts for 6– 18 months, but may recur. Even when the plaques have gone, the skin may retain a rough scaly texture with persistent small scattered follicular plugs. Complications There are usually no complications. However, wide- spread erythroderma causes the patients to tolerate cold poorly. LEARNING POINTS 1 A good diagnostic tip is to look for light reflected from shiny papules. 2 Always look in the mouth. 3 If you can recognize lichen planus, you have pulled ahead of 75% of your colleagues. Fig. 6.8 Pityriasis rubra pilaris. Note the red plugged follicles, seen even in the ‘spared’ areas. CD3C06 21/5/05 11:50 AM Page 67 68 CHAPTER 6 point to look for is the presence of poikiloderma (atrophy, telangiectasia and reticulate pigmentation) in the latter type. Both conditions are stubborn in their response to topical treatment, although often responding temporarily to PUVA. Itching is variable. Complications Patients with suspected premycotic/prelymphomatous eruptions should be followed up carefully, even though the development of cutaneous T-cell lymphoma may not occur for years. If poikiloderma or induration develops, the diagnosis of a cutaneous T-cell lym- phoma becomes likely. Differential diagnosis This includes psoriasis, tinea and nummular (discoid) eczema. In contrast to psoriasis and pityriasis rosea, the lesions of parapsoriasis, characteristically, are asymmetrical. Topical steroids can cause atrophy and confusion. Investigations Several biopsies should be taken if a premycotic erup- tion is suspected, if possible from thick or atrophic untreated areas. These may suggest an early cutaneous T-cell lymphoma, with bizarre mononuclear cells both in the dermis and in microscopic abscesses within the epidermis. Electron microscopy may show abnormal lymphocytes with convoluted nuclei in the dermis or epidermis, although the finding of these cells, especially in the dermis, is non-specific. DNA probes can determine monoclonality of the T cells within the lymphoid infiltrate of mycosis fungoides based on rearrangements of the T-cell receptor genes (p. 19). The use of these probes and of immunophenotyping rather than grossly, and which persist despite anti- psoriasis treatment. It is worth trying to distinguish a benign type of parapsoriasis from a premycotic type, which is a forerunner of mycosis fungoides, a cutaneous T-cell lymphoma (Fig. 6.9)aalthough they can look alike early in their development. However, even the term ‘premycotic’ is disputed, as some think that these lesions are mycosis fungoides right from the start, preferring the term ‘patch stage cutaneous T-cell lymphoma’ (p. 280). Cause The cause is otherwise unknown. Presentation Pink scaly well-marginated plaques appear, typically on the buttocks, breasts, abdomen or flexural skin. The distinguishing features of the small-plaque (benign) and large-plaque (premycotic/prelymphomatous) types are given in Table 6.3. Perhaps the most important Parapsoriasis (benign type) Premycotic/prelymphomatous eruptions Smaller plaques Larger Yellowish Not yellowapink, or slightly violet, or brown Sometimes finger-shaped lesions Asymmetrical with bizarre outline running around the trunk No atrophy Atrophy ± poikiloderma Responds to UVB Responds better to PUVA Remains benign although rarely May progress to a cutaneous T-cell lymphoma clears Fig. 6.9 A bizarre eruption: its persistence and variable colour suggested a prelymphomatous eruption. Biopsy confirmed this. Table 6.3 Distinguishing features of parapsoriasis and premycotic/ prelymphomatous eruptions. CD3C06 21/5/05 11:50 AM Page 68 PAPULOSQUAMOUS DISORDERS 69 the histology is helpful but often it is non-specific. ‘Erythroderma’ is the term used when the skin is red with little or no scaling, while the term ‘exfoliative dermatitis’ is preferred if scaling predominates. Most patients have lymphadenopathy, and many have hepatomegaly as well. If the condition becomes chronic, tightness of the facial skin leads to ectropion, scalp and body hair may be lost, and the nails become thickened and may be shed too. Temperature regula- tion is impaired and heat loss through the skin usually makes the patient feel cold and shiver. Oedema, high output cardiac failure, tachycardia, anaemia, failure to sweat and dehydration can occur. Treatment is that of the underlying condition. Further reading Bhattacharya, M., Kaur, I. & Kumar, B. (2000) Lichen planus: a clinical and epidemiological study. Journal of Dermatology 27, 576–582. Clayton, B.D., Jorrizzo, J.L. & Hitchcock, M.G. (1997) Adult pityriasis rubra pilaris: a 10-year case series. Journal of the American Academy of Dermatology 36, 959–964. Savin, J.A. (1991) Oral lichen planus. British Medical Journal 302, 544–545. helps to differentiate benign parapsoriasis from pre- mycotic/prelymphomatous eruptions. Treatment Treatment is controversial. Less aggressive treatments are used for the benign type of parapsoriasis. Usually, moderately potent steroids or ultraviolet radiation bring some resolution, but lesions tend to recur when these are stopped. For premycotic/prelymphomatous eruptions, treatment with PUVA (p. 59) or with topi- cal nitrogen mustard paints, is advocated by some, although it is not clear that this slows down or pre- vents the development of a subsequent cutaneous T-cell lymphoma. Pityriasis lichenoides Pityriasis lichenoides is uncommon. It occurs in two forms. The numerous small circular scaly macules and papules of the chronic type are easy to confuse with guttate psoriasis (p. 51). However, their scaling is distinctive in that single silver-grey scales surmount the lesions (mica scales). The acute type is characterized by papules that become necrotic and leave scars like those of chickenpox. More often than not there are a few lesions of the chronic type in the acute variant and vice versa. UVB radiation can reduce the number of lesions and spontaneous resolution occurs eventually. Other papulosquamous diseases Discoid lupus erythematosus is typically papulos- quamous; it is discussed with subacute cutaneous lupus erythematosus in Chapter 10. Fungus infec- tions are nummular and scaly and can appear papu- losquamous or eczematous; they are dealt with in Chapter 14. Seborrhoeic and nummular discoid eczema are discussed in Chapter 7. Secondary syphilis is discussed in Chapter 14. Erythroderma/exfoliative dermatitis Sometimes the whole skin becomes red and scaly (see Fig. 5.13). The disorders that can cause this are listed in Table 6.4. The best clue to the underlying cause is a history of a previous skin disease. Sometimes Table 6.4 Some causes of erythroderma/ exfoliative dermatitis. Psoriasis Pityriasis rubra pilaris Ichthyosiform erythroderma Pemphigus erythematosus Contact, atopic, or seborrhoeic eczema Reiter’s syndrome Lymphoma (including the Sézary syndrome) Drug eruptions Crusted (Norwegian) scabies LEARNING POINTS The dangers of erythroderma are the following. 1 Poor temperature regulation. 2 High-output cardiac failure. 3 Protein deficiency. CD3C06 21/5/05 11:50 AM Page 69 70 of these may be in action at the same time (Fig. 7.1). This can make it hard to be sure which type of eczema is present; and even experienced dermatologists admit that they can only classify some two-thirds of the cases they see. To complicate matters further, the physical signs that make up eczema, although limited, can be jumbled together in an infinite number of ways, so that no two cases look alike. The disorders grouped under this heading are the most common skin conditions seen by family doctors, and make up some 20% of all new patients referred to our clinics. Terminology The word ‘eczema’ comes from the Greek for ‘boiling’ aa reference to the tiny vesicles (bubbles) that are often seen in the early acute stages of the disorder, but less often in its later chronic stages. ‘Dermatitis’ means inflammation of the skin and is therefore, strictly speaking, a broader term than eczemaawhich is just one of several possible types of skin inflammation. In the past too much time has been devoted to trying to distinguish between these two terms. To us, they mean the same thing. This approach is now used by most dermatologists, although many stick to the term eczema when talking to patients for whom ‘dermatitis’ may carry industrial and compensation overtones, which can stir up unnecessary legal battles. In this book contact eczema is the same as contact der- matitis; seborrhoeic eczema the same as seborrhoeic dermatitis, etc. Classification of eczema This is a messy legacy from a time when little was known about the subject. As a result, some terms are based on the appearance of lesions, e.g. discoid eczema and hyperkeratotic eczema, while others reflect outmoded or unproven theories of causation, e.g. infective eczema and seborrhoeic eczema. Classification by site, e.g. flexural eczema and hand eczema, is equally unhelpful. Eczema is a reaction pattern. Many different stimuli can make the skin react in the same way, and several 7 Eczema and dermatitis LEARNING POINT ‘When I use a word it means just what I choose it to mean’ said Humpty Dumpty. Choose to make the words eczema and dermatitis mean the same to you. Contact factors Allergens Irritants Epidermis Endogenous factors Fig. 7.1 The causes of eczema. CD3C07 21/5/05 11:49 AM Page 70 ECZEMA AND DERMATITIS 71 help to produce spongiosis (p. 22); and that their secretion by keratinocytes can be elicited by T lym- phocytes, irritants, bacterial products and other stimuli (see Fig. 2.11). Histology (Fig. 7.2) The clinical appearance of the different stages of eczema mirrors their histology. In the acute stage, oedema in the epidermis (spongiosis) progresses to the formation of intraepidermal vesicles, which may co- alesce into larger blisters or rupture. The chronic stages of eczema show less spongiosis and vesication but more thickening of the prickle cell layer (acanthosis) and horny layers (hyperkeratosis and parakeratosis). One time-honoured subdivision of eczema is into exogenous (or contact) and endogenous (or constitu- tional) types. However, it is now clear that this is too simple. Different types of eczema often overlap, e.g. when a contact eczema is superimposed on a gravita- tional one. Even atopic eczema, the type most widely accepted as endogenous, is greatly influenced by external ‘flare factors’aand itself predisposes to the development of irritant contact dermatitis, e.g. caused by soap. Nevertheless, it is still true that any rational approach to any patient with eczema must include a search for remediable environmental factors. A working classification of eczema is given in Table 7.1. Pathogenesis The pathways leading to an eczematous reaction are likely to be common to all subtypes and to involve similar inflammatory mediators (prostaglandins, leukotrienes and cytokines; p. 21). Helper T cells, sometimes activated by superantigens from Staphylo- coccus aureus, predominate in the inflammatory infiltrate. One current view is that epidermal cytokines LEARNING POINT Time spent thinking about contact factors may well help even those patients with the most blatantly ‘constitutional’ types of eczema. Table 7.1 Eczemaaa working classification. Mainly caused by Irritant exogenous (contact) Allergic factors Photodermatitis (Chapter 16) Other types of eczema Atopic Seborrhoeic Discoid (nummular) Pompholyx Gravitational (venous, stasis) Asteatotic Neurodermatitis Juvenile plantar dermatosis Napkin (diaper) dermatitis Vesication Weeping Crusting Chronic lichenification Fig. 7.2 The sequence of histological events in eczema. CD3C07 21/5/05 11:49 AM Page 71 72 CHAPTER 7 These changes are accompanied by a variable degree of vasodilatation and infiltration with lymphocytes. Clinical appearance The different types of eczema have their own distin- guishing marks, and these will be dealt with later; most share certain general features, which it is con- venient to consider here. The absence of a sharp mar- gin is a particularly important feature that separates eczema from most papulosquamous eruptions. Acute eczema Acute eczema (Figs 7.3 and 7.4) is recognized by its: • weeping and crusting; • blisteringausually with vesicles but, in fierce cases, with large blisters; • redness, papules and swellingausually with an ill- defined border; and • scaling. Chronic eczema Chronic eczema may show all of the above changes but in general is: • less vesicular and exudative; • more scaly, pigmented and thickened; • more likely to show lichenification (Fig. 7.5)aa dry leathery thickened state, with increased skin markings, secondary to repeated scratching or rubbing; and • more likely to fissure. Fig. 7.3 Acute vesicular contact eczema of the hand. Fig. 7.4 Vesicular and crusted contact eczema of the face (cosmetic allergy). Fig. 7.5 Lichenification of the wristsanote also the increased skin markings on the palms (‘atopic palms’). LEARNING POINTS 1 Eczema is like jazz; it is hard to defineabut it should be easy to recognize if you bear in mind the physical signs listed above. 2 If it does not itch, it is probably not eczema. CD3C07 21/5/05 11:49 AM Page 72 ECZEMA AND DERMATITIS 73 family life. Eczema can interfere with work, sporting activities and sex lives. Jobs can be lost through it. Differential diagnosis This falls into two halves. First, eczema has to be separated from other skin conditions that look like it. Table 7.2 plots a way through this maze. Always Complications Heavy bacterial colonization is common in all types of eczema but overt infection is most troublesome in the seborrhoeic, nummular and atopic types. Local sup- erimposed allergic reactions to medicaments can pro- voke dissemination, especially in gravitational eczema. All severe forms of eczema have a huge effect on the quality of life. An itchy sleepless child can wreck Table 7.2 Is the rash eczematous? Atypical physical signs? Could be eczema but consider other erythemato- squamous eruptions ↓ Sharply marginated, strong colour, very scaly? Points of elbows and knees involved? ↓No Itchy social contacts? Face spared? Burrows found? Genitals and nipples affected? ↓No Mouth lesions? Violaceous tinge? Shiny flat topped papules? ↓No Annular lesions with active scaly edges? ↓No Localized to palms and soles? Obvious pustules? ↓No Unusually swollen; on the face? ↓No Consider dermatitis herpetiformis, not the various pityriases (rosea, versicolor, and rubra pilaris) and drug eruptions (Chapter 22) → → → → → → Likely to be psoriasis (Chapter 5) This is scabies (p. 227) Could be lichen planus (p. 64) Probably a fungal infection (Chapter 14) Probably palmoplantar pustulosis (p. 53) Consider angioedema (p. 97) or erysipelas (p. 192) Yes → Yes → Yes → Yes → Yes → Yes → Can be confused with seborrhoeic eczema and neurodermatitis on the scalp, with seborrhoeic eczema in the flexures, and discoid eczema on the limbs. Look for confirmatory nail and joint changes. Ask about family history Ensure all contacts are treated adequatelya whether itchy or not Also consider lichenoid drug eruptions More likely if the rash affects the groin, or is asymmetrical, perhaps affecting the palm of one hand only; and not doing well with topical steroids. Look at scales, cleared with potassium hydroxide, under a microscope or send scrapings to mycology laboratory. Check for contact with animals and for thickened toe nails Expect poor response to most topical treatments Needs rapid treatment with antihistamines or antibiotics CD3C07 21/5/05 11:49 AM Page 73 74 CHAPTER 7 standardized allergens (see Fig. 3.7). Patch testing can be used to confirm a suspected allergy or, by the use of a battery of common sensitizers, to discover unsus- pected allergies, which then have to be assessed in the light of the history and the clinical picture. A visit to the home or workplace may help with this. Photopatch testing is more specialized and facilities are only available in a few centres. A chemical is applied to the skin for 24 h and then the site is irradiated with a suberythema dose of ultraviolet irradiation; the patches are inspected for an eczematous reaction 48 h later. Other types of eczema The only indication for patch testing here is when an added contact allergic element is suspected. This is most common in gravitational eczema; neomycin, framycetin, lanolin or preservative allergy can per- petuate the condition and even trigger dissemination. Ironically rubber gloves, so often used to protect eczematous hands, can themselves sensitize. The role of prick testing in atopic eczema is dis- cussed on p. 36. Patients with atopic dermatitis often have multiple type I reactions to foods, danders, pollens, dusts and moulds. Some find the measurement of serum total immunoglobulin E (IgE), and of IgE antibodies specific to certain antigens, not only useful in diagnosing the atopic state, but also helpful when advising on the role of dietary and environmental allergens in causing or perpetuating atopic dermatitis, particularly in chil- dren. Total and specific IgE antibodies are measured by a radioallergosorbent test (RAST). Prick and RAST testing give similar results but many now prefer the more expensive RAST test as it carries no risk of anaphyl- axis, is easier to perform and is less time consuming. If the eczema is worsening despite treatment, or if there is much crusting, heavy bacterial colonization may be present. Opinions vary about the value of cultures for bacteria and candida, but antibiotic treatment may be helpful. Scrapings for microscopical examination (p. 35) and culture for fungus will rule out tinea if there is clinical doubtaas in some cases of discoid eczema. Finally, malabsorption should be considered in otherwise unexplained widespread pigmented atypical patterns of endogenous eczema. remember that eczemas are scaly, with poorly defined margins. Occasionally a biopsy is helpful in confirming a diagnosis of eczema, but it will not determine the cause or type. Once the diagnosis of eczema becomes solid, look for clinical pointers towards an external cause. This determines both the need for investiga- tions and the best line of treatment. Sometimes an eruption will follow one of the well-known patterns of eczema, such as the way atopic eczema picks out the skin behind the knees, and a diagnosis can then be made readily enough. Often, however, this is not the case, and the history then becomes especially important. A contact element is likely if: • there is obvious contact with known irritants or allergens; • the eruption clears when the patient goes on holiday, or at the weekends; • the eczema is asymmetrical, or has a linear or recti- linear configuration; or • the rash picks out the eyelids, external ear canals, hands and feet, the skin around stasis ulcers, or the peri-anal skin. Investigations Each pattern of eczema needs a different line of inquiry. Exogenous eczema Here the main decision is whether or not to under- take patch testing (p. 35) to confirm allergic contact dermatitis and to identify the allergens responsible for it. In patch testing, standardized non-irritating con- centrations of common allergens are applied to the normal skin of the back. If the patient is allergic to the allergen, eczema will develop at the site of contact after 48–96 h. Patch testing with irritants is of no value in any type of eczema, but testing with suitably diluted allergens is essential in suspected allergic con- tact eczema. The technique is not easy. Its problems include separating irritant from allergic patch test reactions, and picking the right allergens to test. If legal issues depend on the results, testing should be carried out by a dermatologist who will have the stan- dard equipment and a suitable selection of properly CD3C07 21/5/05 11:49 AM Page 74 ECZEMA AND DERMATITIS 75 the skin and provides rapid relief of itching. With improvement, the frequency of the dressings can be cut down and a moisturiser can be substituted for the corticosteroid. Parents can be taught the technique by a trained nurse, who must follow up treatment closely. Parents easily learn how to modify the tech- nique to suit the needs of their own child. Side-effects seem to be minimal. Subacute eczema Steroid lotions or creams are the mainstay of treat- ment; their strength is determined by the severity of the attack. Vioform, bacitracin, fusidic acid, mupirocin or neomycin (see Formulary 1, p. 334) can be incor- porated into the application if an infective element is present, but watch out for sensitization to neomycin, especially when treating gravitational eczema. Chronic eczema This responds best to steroids in an ointment base, but is also often helped by non-steroid applications such as ichthammol and zinc cream or paste. The strength of the steroid is important (Fig. 7.6). Nothing stronger than 0.5 or 1% hydrocortisone ointment should be used on the face or in infancy. Even in adults one should be reluctant to prescribe more than 200 g/week of a mildly potent steroid, 50 g/week of a moderately potent or 30 g/week of a potent one for long periods. Very potent topical steroids should not be used long-term. Treatment Acute weeping eczema This does best with rest and liquid applications. Non- steroidal preparations are helpful and the techniques used will vary with the facilities available and the site of the lesions. In general practice a simple and con- venient way of dealing with weeping eczema of the hands or feet is to use thrice daily 10-min soaks in a cool 0.65% aluminium acetate solution (Formulary 1, p. 329)asaline or even tap water will do almost as wellaeach soaking being followed by a smear of a corticosteroid cream or lotion and the application of a non-stick dressing or cotton gloves. One reason for dropping the dilute potassium permanganate solution that was once so popular is because it stains the skin and nails brown. Wider areas on the trunk respond well to cortico- steroid creams and lotions. However, traditional rem- edies such as exposure and frequent applications of calamine lotion, and the use of half-strength magenta paint for the flexures are also effective. An experienced doctor or nurse can teach patients how to use wet dressings, and supervise this. The aluminium acetate solution, saline or water, can be applied on cotton gauze, under a polythene covering, and changed twice daily. Details of wet wrap tech- niques are given below. Rest at home will help too. Wet wrap dressings This is a labour-intensive, but highly effective tech- nique, of value in the treatment of troublesome atopic eczema in children. After a bath, a corticosteroid is applied to the skin and then covered with two layers of tubular dressingathe inner layer already soaked in warm water, the outer layer being applied dry. Cotton pyjamas or a T-shirt can be used to cover these, and the dressings can then be left in place for several hours. The corticosteroid may be one that is rapidly metabolized after systemic absorption such as a beclomethasone (beclometasone) diproprionate oint- ment diluted to 0.025% (available only in the UK). Alternatives include 1 or 2.5% hydrocortisone cream for children and 0.025 or 0.1 % triamcinolone cream for adults. The bandages can be washed and reused. The evaporation of fluid from the bandages cools Fig. 7.6 Stretch marks following the use of too potent topical steroids to the groin. CD3C07 21/5/05 11:49 AM Page 75 [...]... protective ointments, are often useful ECZEMA AND DERMATITIS 93 LEARNING POINTS Fig 7 .30 Irritant napkin erythema with a hint of sparing of the skin folds (Formulary 1, p 33 1), as are topical imidazole preparations that stop yeast growth Potent steroids should be avoided but combinations of hydrocortisone with antifungals or antiseptics (Formulary 1, p 33 2) are often useful Further reading Bieber, T and Leung,... look highly impressive Topical tacrolimus is now available as Protopic ointment (Formulary 1, p 33 4) Pimecrolimus (Formulary 1, p 33 4) is another topical immunosuppressant and a derivative of askamycin Clinical trials in moderate atopic eczema have been encouraging and it can be used in patients older than 3 months Its action is very similar to that of tacrolimus and time will tell if either preparation... tissue 3 6 h later The swelling 96 CHAPTER 8 FcIgE receptors on mast cells Here the autoantibody acts as antigen to trigger mast cell degranulation Pharmacological urticaria This occurs when drugs cause mast cells to release histamine in a non-allergic manner (e.g aspirin, non-steroidal anti-inflammatory drugs (NSAIDs), angiotensin-converting enzyme (ACE) inhibitors and morphine) Contact urticaria Fig 8 .3. .. 1, p 33 5) are perhaps the first line of treatment Two per cent sulphur and 2% salicylic acid in aqueous cream is often helpful and avoids the problem of topical steroids It may be used on the scalp overnight and removed by a medicated shampoo, which may contain ketoconazole, tar, salicylic acid, sulphur, zinc or selenium sulphide (Formulary 1, p 32 9) A topical lithium preparation (Formulary 1, p 33 9)... are allergens Mercapto-mix Chemicals used to harden rubber Diagnosis is often obvious: sometimes less so Remember shoe soles, rubber bands and golf club grips Thiuram-mix Another set of rubber accelerators Common culprit in rubber glove allergy Black rubber mix All black heavy-duty rubber, e.g tyres, rubber boots, squash balls These are paraphenylene diamine derivatives, cross-reacting with PPD dyes... and to spot the less common ones in the environment needs specialist knowledge Table 7 .3 lists some common allergens and their distribution Allergic contact dermatitis should be suspected if: 1 certain areas are involved, e.g the eyelids, external auditory meati, hands (Fig 7.10) or feet, and around gravitational ulcers; 2 there is known contact with the allergens mentioned in Table 7 .3; or 3 the individual’s... type II response (see Chapter 2) and are poor at producing γ-interferon (IFN-γ); this persists into late childhood Early infections may lower the risk of allergy by boosting the production of INF-γ One promising but still experimental way of tackling these problems has emerged recently, involving the use of probiotics, which are cultures of potentially beneficial bacteria They may reverse the increased... prescriptions of topical steroids, keeping an eye on the amount used and their potency 4 Do not promise that atopic eczema will be clear by any particular age: guesses are always wrong and the patients lose faith Hanifin, J and Saurat, J.-H (2001) Understanding atopic dermatitis pathophysiology and etiology Journal of the American Academy of Dermatology, Suppl 45/1 Hanifin, J.M (2001) 1996 Tacrolimus ointment:... ointment: advancing the treatment of atopic dermatitis Journal of the American Academy of Dermatology, Suppl 44/1 Kanerva, L., Elsner, P., Wahlberg, J.E & Maibach, H.I (2000) Handbook of Occupational Dermatology Springer, Berlin Rycroft, R.J.G., Menne, T., Frosch, P & Lepoittevin, J.-P (2001) Textbook of Contact Dermatitis, 3rd edn Springer, Berlin 8 Reactive erythemas and vasculitis Blood vessels can be... systemic side-effects In primary care, avoid using potent and very potent steroids for children with atopic eczema Be wary of repeat prescriptions 86 CHAPTER 7 Table 7.7 Winning ways with emollients Make sure they are applied when the skin is moist Prescribe plenty (at least 500 g/week for the whole skin of an adult and 250 g/week for the whole skin of a child) and ensure they are used at least 3 4 times . 200 g/week of a mildly potent steroid, 50 g/week of a moderately potent or 30 g/week of a potent one for long periods. Very potent topical steroids should not be used long-term. Treatment Acute. blockers, non-steroidal anti-inflammatory drugs, para-aminobenzoic acid, thiazide diuretics and peni- Hyperkeratosis Prominent granular layer Basal cell degeneration Sawtooth dermo- epidermal junction Colloid. own distin- guishing marks, and these will be dealt with later; most share certain general features, which it is con- venient to consider here. The absence of a sharp mar- gin is a particularly