Management of atopic eczema

Dr Chandana Chandran 

INTRODUCTION ^[1]
Eczema, or dermatitis, is a reaction pattern that presents with variable clinical and histologic findings and is the final common expression for a number of disorders, including atopic dermatitis, allergic contact and irritant contact dermatitis, dyshidrotic eczema, nummular eczema, lichen simplex chronicus, asteatotic eczema, and seborrheic dermatitis. Primary lesions may include papules, erythematous macules, and vesicles, which can coalesce to form patches and plaques. In severe eczema, secondary lesions from infection or excoriation, marked by weeping and crusting, may predominate. Long-standing dermatitis is often dry and is characterized by thickened, scaling skin (lichenification).

DEFINITION ^[2]

• Atopic dermatitis is a difficult condition to define because it lacks a diagnostic test and shows variable clinical features. The following definition seems to be in accord with most consensus groups. Atopic dermatitis (which is synonymous with atopic eczema) is an itchy, chronic, or chronically relapsing, inflammatory skin condition. The rash is characterized by itchy papules (occasionally vesicles in infants) which become excoriated and lichenified, and typically have a flexural distribution. The eruption is frequently associated with other atopic conditions in the individual or other family members.

Atopic and non-atopic dermatitis

One of the difficulties in defining atopic dermatitis arises from the impreciseness of its association with atopy and the nature of atopy itself. Atopic dermatitis and disorders resulting from anaphylaxis, for example those resulting from insect stings and food allergies, may be associated with IgE antibodies and therefore grouped with the atopic diseases. Such grouping is not completely acceptable, as 20–40% of individuals with atopic dermatitis can have a normal total or specific IgE level, and it is rarely attributable to a specific allergic reaction; the IgE antibodies present in the blood often appear to be incidental to the condition.

It is still a matter of debate whether the group with dermatitis and normal IgE levels, termed intrinsic atopic dermatitis or nonatopic dermatitis, can be distinguished clinically, immunologically, and prognostically from extrinsic or atopic dermatitis. Upto 50% of infants have been reported to have intrinsic dermatitis, but with time atopic features become more prevalent and the intrinsic form may be found in only 5.4% of adult patients ^[2].

• Atopy is a genetic predisposition to form excessive IgE which leads to a generalized and prolonged hypersensitivity to common environmental antigens, including pollen and the house dust mite. Atopic individuals manifest one or more of a group of disease that includes asthma, hay fever, urticaria, food and other allergies, and this distinctive form of eczema. These atopic conditions tend to run true to type within each family ^[3].

DIAGNOSTIC CRITERIA ^[2]

Hanifin and Rajka proposed major and minor diagnostic criteria based on their clinical experience. These criteria allow a uniformity of diagnosis for hospital-based and experimental studies but were considered not helpful for population-based studies. Consequently, Williams coordinated a UK working party to attempt to refine the criteria of Hanifin and Rajka into a repeatable and validated set of diagnostic criteria for atopic dermatitis.

These diagnostic guidelines appear to be valid for adults, children and non-white ethnic groups suffering from atopic dermatitis, and have been validated in a population setting. They were primarily developed for epidemiological studies and, of necessity, exclude some signs that could be useful for diagnosis in individuals but are not common enough for use when assessing large populations.

More recently, other modifications of the diagnostic criteria have been proposed, but these have been less rigorously validated.

In order to qualify as a case of atopic dermatitis with the UK diagnostic criteria, the child must have:

• An itchy skin condition (or parental report of scratching or rubbing in a child)

Plus three or more of the following:

1. Onset below age 2 years (not used if child is under 4 years)
2. History of skin crease involvement (including cheeks in children under 10 years)
3. History of a generally dry skin
4. Personal history of other atopic disease (or history of any atopic disease in a first degree relative in children under 4 years)
5. Visible flexural dermatitis (or dermatitis of cheeks/forehead and outer limbs in children under 4 years).

AETIOLOGY ^[3]

The inheritance of atopic eczema is controversial. The disorder is concordant in 86% of monozygotic twins but only in 21% of dizygotes. Atopic diseases show maternal imprinting- that is, they are inherited more often from the mother than from the father. A polygenic mode of inheritance is likely. More than one genetic locus has been identified that might play a role in the inheritance of atopy and more specifically atopic eczema.

The prevalence of atopic eczema is increasing and has increased between two and five fold over the last 30 years. It now affects 1 in 10 schoolchildren. Environmental factors, such as exposure to allergens either in utero or during childhood, have been shown to have a role in the etiology of atopic eczema.

The pathogenesis of atopic eczema is complex and still incompletely understood. It is best considered as interplay of genetic susceptibility that causes epidermal barrier dysfunction and abnormal immune responses, which are then stimulated by different environmental factors ^[3].

The etiology of atopic eczema is only partially defined, but there is a clear genetic predisposition. When both parents are affected byatopic eczema, over 80% of their children manifest the disease. When only one parent is affected, the prevalence drops to slightly over 50%. Patients with atopic eczema may display a variety of immunoregulatory abnormalities including increased IgE synthesis; increased serum IgE; increased specific IgE to foods, aeroallergens, bacteria, and bacterial products; increased expression of CD23 (low-affinity IgE receptor) on monocytes and B cells; and impaired delayed type hypersensitivity reactions.

The clinical presentation often varies with age. Half of patients with Atopic eczema present within the first year of life, and 80% present by 5years of age. About 80% ultimately coexpress allergic rhinitis or asthma. The infantile pattern is characterized by weeping inflammatory patches and crusted plaques that occur on the face, neck, and extensor surfaces. The childhood and adolescent pattern is marked by dermatitis of flexural skin, particularly in the antecubital and popliteal fossae. Atopic eczema may resolve spontaneously, but over half of all individuals affected as children will have dermatitis in adult life. The distribution of lesions may be similar to those seen in childhood. However, adults frequently have localized disease, manifesting as hand eczema or lichen simplex chronicus. In patients with localized disease, atopic eczema may be suspected because of a typical personal history, family history, or the presence of cutaneous stigmata of atopic eczema such as perioral pallor, an extra fold of skin beneath the lower eyelid (Dennie’s line), increased palmar skin markings, and an increased incidence of cutaneous infections, particularly with Staphylococcus aureus. Regardless of other manifestations, pruritus is a prominent characteristic of atopic eczema and is exacerbated by dry skin. Many of the cutaneous findings in affected patients, such as lichenification, are secondary to rubbing and scratching.

Histologic examination of the skin affected by atopic eczema may demonstrate features of acute or chronic dermatitis. Immunopathology shows activated, memory T helper cells. Atopic eczema skin lesions may also demonstrate IgE-bearing CD1a+Langerhans cells, and these cells have been implicated in atopic eczema disease pathophysiology through mediation of hypersensitivity responses to environmental antigens ^[1].

CLINICAL FEATURES ^[2]

Atopic dermatitis is an itchy, chronic, fluctuating disease that is slightly more common in boys than girls, with a range of clinical features. The age of onset is between 2 and 6 months in the majority of cases, but it may start at any age, even before the age of 2 months in some cases. The distribution of the eruption varies with age, as described below.

• INFANTILE PHASE

The lesions most frequently start on the face, but may occur anywhere on the skin surface. Often, the napkin area is relatively spared. When the child begins to crawl, the exposed surfaces, especially the extensor aspect of the knees, are most involved. The lesions consist of erythema and discrete or confluent oedematous papules. The papules are intensely itchy, and may become exudative and crusted as a result of rubbing. Secondary infection and lymphadenopathy are common. The disease runs a chronic, fluctuating course, varying with such factors as teething, respiratory infections, emotional upsets and climatic changes.

• CHILDHOOD PHASE

From 18 to 24 months onwards, the sites most characteristically involved are the elbow and knee flexures, sides of the neck, wrists and ankles. The sides of the neck may show a striking reticulate pigmentation, sometimes referred to as ‘atopic dirty neck’. The anatomical basis for this distribution is unknown. Sometimes only one site is involved. The erythematous and oedematous papules tend to be replaced by lichenification. Some patients with atopic dermatitis are apparently unable to lichenify, even after prolonged rubbing, and they may be very difficult to treat. Patients with an extensor distribution of eczema in later childhood are uncommon, and may take longer to remit. This distribution is said to be commoner in Asian or black children, but frequently they show the typical distribution. As well as the typical mixture of papules and lichenification, true eczematous lesions with vesiculation may occur, often in discoid patches. Involvement of the hands, often with exudative lesions, and sometimes with nail changes, is common. Acute generalized or localized vesiculation should always suggest the possibility of secondary bacterial or viral infection.

• ADULT PHASE

The picture is essentially similar to that in later childhood, with lichenification, especially of the flexures and hands. Localized patches of atopic dermatitis can occur on the nipples, especially in adolescent and young women. Involvement of the vermilion of the lips and the adjacent skin is commonly an atopic manifestation. Follicular lichenified papules are a frequent feature in black people and the Japanese. A distribution on the face, upper arms and back may correlate with areas of maximal thermal sweating or Malassezia sensitivity. Photosensitivity is not uncommon, especially in adults with atopic dermatitis. The mechanisms involved are several and complex. Many such cases do not show sensitivity when tested with the monochromator. Rajka has suggested that infrared and UV radiation may both contribute. Management of such cases requires a combination of approaches used for ordinary atopic dermatitis and for photosensitivity neither alone sufficing.

• ATOPIC HAND ECZEMA

The prevalence of hand eczema in patients with active atopic dermatitis was 58.9% in a recent study, and the prevalence rises with increasing age. A patchy, somewhat vesicular and lichenified eczema is a common manifestation of atopic dermatitis in childhood. The nails are often involved, resulting in coarse pitting and ridging. A more diffuse, chronic lichenified eczema of the hands is frequently found in cases of extensive atopic dermatitis which persist into adult life, and atopic dermatitis is frequently a contributory factor in many cases of what usually has to be called constitutional hand eczema. A previous history of atopic dermatitis, and more particularly hand involvement, is a highly significant risk factor for the development of occupational dermatitis. Involvement of the feet is also common and almost half the patients with atopic hand eczema will have eczema on the feet.

ASSOCIATED DISORDERS ^[2]

• OTHER MANIFESTATIONS OF ATOPY

Allergic rhinitis(hay fever) and asthma. They occur in 30–50% of cases atopic dermatitis. Atopic dermatitis is a risk factor for the future development of allergic airways disease, possibly by percutaneous sensitization to protein antigen. The age of onset is later than that of the eczema. Latent asthma may be detected by bronchial inhalation tests in a proportion of patients with atopic dermatitis without clinical asthma.

• DRY SKIN

This is a common feature of atopic dermatitis and figures prominently in its management. It is likely that it occurs because of increased trans-epidermal water loss through an abnormal stratum corneum, which may also correlate with disease activity. The dry skin may be a consequence of abnormal ceramide synthesis and have an important role in the development of inflammation. Ceramide-containing emollients may be helpful in managing the condition. Ichthyosis vulgaris and keratosis pilaris may also be seen in association with the condition and loss-of-function variants of the barrier protein filaggrin may be the link between these conditions and atopic dermatitis.

COMPLICATIONS ^[2]

• PSYCHOSOCIAL ASPECTS

Atopic dermatitis has a profound effect, equal to or greater than that of asthma and diabetes, on many aspects of patients lives and the lives of their families. In children, the most troublesome symptoms are itching, distress at bath time and difficulty going to sleep. This can lead to behavioural difficulties in severely affected children. The patient’s dermatitis promotes family dysfunction, causing exhaustion, sleep deprivation and emotional distress. Increasingly, a demonstration of improvement in the quality of life of patients forms part of the assessment of new therapies and reveal that advice from experienced teams can improve well-being.

• GROWTH DELAY

Growth delay can be associated with atopic dermatitis. It used to be seen in severe cases before the advent of corticosteroid therapy, and can therefore be attributed to the disease. However, suspicion must also clearly rest on both oral and topical steroid therapy, which can cause growth stunting in any child on longterm therapy. Prepubertal children with atopic dermatitis show features consistent with constitutional growth delay.

• BACTERIAL INFECTIONS

Secondary bacterial infection with staphylococci or streptococci is virtually an integral part of the clinical picture. It contributes to many exacerbations of the disease, even without grossly visible purulent exudate. Widespread impetigo may sometimes closely mimic Kaposi’s varicelliform eruption. Indeed, any acute vesicular eruption in an atopic should suggest the diagnosis of secondary bacterial or viral infection.

• VIRAL INFECTIONS

Patients with atopic dermatitis, both active and quiescent, are liable to develop acute generalized infections with herpes simplex virus (eczema herpeticum), to produce the clinical picture of Kaposi’s varicelliform eruption. Such episodes may present as a severe systemic illness with high fever and a widespread eruption. However, there may be no systemic disturbance, and at times the eruption may be quite localized, often to areas of pre-existing atopic dermatitis. The individual lesions start as the characteristic viral papulovesicles, but not necessarily with an herpetiform grouping. There may then be rapid evolution to a state in which extensive purulent exudate masks the initial papulovesicles, or superficial scattered erosions may be the only clue to the cause of a rapid deterioration of the dermatitis. The differential diagnosis includes bacterial impetigo and chickenpox. Herpes zoster and chickenpox apparently behave as in normal persons.

There is a lack of agreement about whether viral warts are more prevalent in atopic dermatitis. An initial uncontrolled study suggested an increased frequency of viral wart infections, but a more recent epidemiological study has cast doubt on this observation.

Similarly, the frequency of molluscum contagiosum in such patients is not clear. However, the clinical impression is that widespread molluscum contagiosum is more common in the atopic child.

An abnormal response to a Coxsackie infection in an atopic has been described. AIDS may aggravate atopic dermatitis, and ‘recall’ atopic dermatitis has been described in AIDS patients. A condition resembling atopic dermatitis has been seen in association with HTLV-1 infection, although this may be coincidental.

• OCULAR ABNORMALITIES

A number of ocular changes can occur in atopic dermatitis. The Dennie–Morgan fold is often present as a fold of skin under the lower eyelids. However, this change is not specific to atopic dermatitis, and is commonly seen in non-atopic black children.

Conjunctival irritation is a common syndrome in atopic persons. As in hay fever it may represent a true allergic reaction, or it may be due to a non-allergic irritability such as occurs in the nose or skin. Keratoconjunctivitis has been recorded.

Keratoconus, or conical cornea, is a rare condition. It may occur in the absence of any other disease or in association with atopic dermatitis. It is due to a degenerative change in the cornea, which is forced outwards by the intraocular pressure, to give rise to marked visual disturbances. Onset is in childhood, and after some years progress of the disease becomes arrested. Contact lenses may be helpful.

Cataract associated with atopic dermatitis has certain peculiarities which distinguish it from other types of cataract. It occurs in up to 10% of the more severe adolescent and adult cases, but overall it is uncommon. It is associated with atopic dermatitis rather than with other atopic diseases perhaps because of a genetic risk factor. It may start in early childhood or up to the age of 30 years, but the peak incidence is between 15 and 25 years. It is almost always bilateral. The appearances on slitlamp examination are characteristic but not diagnostic. In the early stages translucent globules and small opacities appear at the pole in front of the posterior capsule and also in the anterior subcapsular zone. Progression may be slow, or alarmingly rapid over a few days, and seems to be related to severe facial involvement. The final appearance may resemble a mature, cortical, senile cataract.

Atopic cataracts may resemble those induced by topical or systemic steroids. The potential for cataract formation is an important reason for examining the eyes of any patient with atopic dermatitis when psoralen and UVA (PUVA) therapy is being contemplated.

Retinal detachment has been reported, particularly in Japanese patients, and appears to be identical to the retinal detachment seen following trauma.

NATURAL HISTORY AND PROGNOSIS ^[2]

Hospital-based studies suggest the age of onset is less than 6 months in 75% of cases and before the age of 5 years in 80–90%. However, community-ascertained cases may have a later age of onset than that reported in hospital-based studies. The reported prognosis differs considerably according to how the cases are selected, the criteria for diagnosis and many other variables. There is a general tendency towards spontaneous improvement throughout childhood and often some slight relapse during adolescence.

Relatively few typical cases persist over the age of 30 years; perhaps half of all cases clear by the age of 13 years. The reported clearance rates range from 40 to 60% within 10–20 years; 84% within 5–20 years; and 50% at 10 years.

It is difficult to predict the prognosis in an individual case. However, children with severe disease, starting early, who also have asthma, hay fever and a family history of atopic dermatitis are likely to have more persistent disease. Children with raised IgE antibodies to foods and inhalant antigens at 2 years of age may also have a poorer prognosis.

Recently, it has been suggested that involvement of the head and neck of adults implies further prolonged disease. In addition, the atopic patient remains particularly at risk from occupational irritant hand dermatitis as an adult.

DIFFERENTIAL DIAGNOSIS ^[2]

In the individual patient, one must consider a number of other conditions. Scabies should always be excluded, and can cause confusion when superimposed on pre-existing atopic dermatitis. In the fi rst few months of life the differentiation of infantile seborrhoeic dermatitis from atopic dermatitis can be difficult, although with time the distinction becomes apparent. Immunodeficiency states should also be considered in infants in whom the disease is unusually severe, when there are recurrent systemic or ear infections, and if there is failure to thrive, malabsorption or petechiae. Recurrent infected eczema in Jamaican children may be associated with HTLV-1 infection. An eruption resembling atopic dermatitis, with or without other atopic disorders, and sometimes with raised IgE levels, may be found in several genetic and metabolic disorders. In adults, flexural eczema may be a consequence of secondary dissemination of other types of eczema, for example in nickel allergy and occupational contact dermatitis.

• HYPER-IGE SYNDROME

This is a syndrome that develops in infants or children. It resembles atopic dermatitis, but tends to involve particularly the scalp, axillae and groins. It may be inherited in an autosomal dominant or autosomal recessive form. In the dominant inheritance the associated features include persistent secondary bacterial infection, fluctuant cold abscesses, contact urticaria, bronchitis and more severe lung damage. The recessive disease has a broader range of bacterial infections along with severe chronic molluscum contagiosum and herpes infections. The key laboratory finding is the great elevation of serum IgE levels (greater than 200 i.u./mL), often with some eosinophilia. Other immunoglobulins are often normal in the dominant form but elevated in the recessive variant.

• HYPEREOSINOPHILIC SYNDROME

Eosinophilia is a common feature of many diseases, including several skin diseases. In this situation the eosinophilia is reactive and induced as a response to eosinophilopoietic cytokines. However, clonal eosinophilia may present with skin signs, including: a non-specific, itchy, maculopapular eruption; urticaria or angio-oedema; an eruption resembling atopic dermatitis; or erythroderma. Only a few such cases can be attributed to an eosinophil leukaemia. The clinical manifestations appear to be attributable to the eosinophilia itself, and include cardiac involvement, and involvement of the nervous system, liver, lungs and gut.

• PACHYDERMATOUS EOSINOPHILIC DERMATITIS

A generalized rash associated with marked blood and skin eosinophilia, and called it hypereosinophilic dermatitis. More recently, a variant of this disorder has been described in three black South African teenage girls, and designated pachydermatous eosinophilic dermatitis. This condition is thought to resemble severe atopic dermatitis or onchodermatitis. However, the three patients had peculiar hypertrophic genital lesions, peripheral blood eosinophilia and an eosinophil-rich lymphohistiocytic cutaneous infiltrate.

INVESTIGATIONS ^[2]

The diagnosis of atopic dermatitis is rarely aided by investigations. Estimation of total serum IgE, specific radioallergosorbent tests (RASTs) and prick tests usually serve only to confirm the atopic nature of the individual. It is possible that such confirmation may be of value occasionally in adult-onset dermatitis. However, one must remember that 20% of patients with atopic dermatitis have normal total IgE levels and negative RASTs, whereas 15% of apparently healthy individuals have a raised IgE.

The value of investigations in identifying trigger factors in atopic dermatitis is disputed. How helpful specific RASTs to foods or aeroallergens are for disease management is unclear, although it is suggested that if they are negative allergy is unlikely. It may be that skin prick test positivity to food allergens in young children with severe atopic dermatitis and a high serum IgE indicates a high risk of developing later allergic respiratory disease [6]. Adults with head and neck dermatitis and positive RASTs to Malassezia species may benefit from treatment with oral anti-yeast therapies.

If one suspects immunodeficiency with atopic dermatitis, then the appropriate investigations should be performed, for example immunoglobulin levels and subclasses, IgE levels, white-cell count, platelets, complement levels and function, and T, B and phagocyte cell numbers and functions. If clinically appropriate, one may also consider testing for HTLV-1 and HIV.

Bacteriology and virology swabs may be helpful in identifying causes for deterioration of atopic dermatitis. Although atopic dermatitis skin is often colonized by Staphylococcus aureus, bacterial\ culture can identify antibiotic resistance and detect β–haemolytic streptococci. Herpes simplex is usually readily cultured, but a Tzanck smear, an immunofluorescence slide test or electron microscopy can also be helpful, and will provide more rapid confirmation of infection.

Patch testing may also help to identify a contact allergen responsible for deterioration of the skin condition, particularly in adults. The ‘atopy patch test’ for aeroallergens and foods in atopic dermatitis, and the skin-application food test (SAFT) in the management of the IgE-mediated contact urticaria syndrome in children with atopic dermatitis, are recommended by some authorities.

TREATMENT ^[4]

Atopic dermatitis can be persistent. You may need to try various treatments over months or years to control it. And even if treatment is successful, signs and symptoms may return (flare).It’s important to recognize the condition early so that you can start treatment. If regular moisturizing and other self-care steps don’t help, your doctor may suggest one or more of the following treatments:

• MEDICATIONS

• Creams that control itching and help repair the skin.Your doctor may prescribe a corticosteroid cream or ointment. Apply it as directed, after you moisturize. Overuse of this drug may cause side effects, including thinning skin.

Other creams containing drugs called calcineurin inhibitors — such as tacrolimus (Protopic) and pimecrolimus (Elidel) — affect your immune system. They are used by people older than age 2 to help control the skin reaction. Apply it as directed, after you moisturize. Avoid strong sunlight when using these products.

These drugs have a black box warning about a potential risk of cancer. But the American Academy of Allergy, Asthma & Immunology has concluded that the risk-to-benefit ratios of topical pimecrolimus and tacrolimus are similar to those of most other conventional treatments of persistent eczema and that the data don’t support the use of the black box warning.

• Drugs to fight infection.Your doctor may prescribe an antibiotic cream if your skin has a bacterial infection, an open sore or cracks. He or she may recommend taking oral antibiotics for a short time to treat an infection.
• Oral drugs that control inflammation.For more-severe cases, your doctor may prescribe oral corticosteroids — such as prednisone. These drugs are effective but can’t be used long term because of potential serious side effects.
• Newer option for severe eczema.The Food and Drug Administration (FDA) has recently approved a new, injectable biologic (monoclonal antibody) called dupilumab (Dupixent). It is used to treat people with severe disease who do not respond well to other treatment options. This is a newer medication, so it doesn’t have a long track record in terms of how well it helps people. Studies have shown it to be safe if used as directed. It is very expensive.
• THERAPIES
• Wet dressings.An effective, intensive treatment for severe atopic dermatitis involves wrapping the affected area with topical corticosteroids and wet bandages. Sometimes this is done in a hospital for people with widespread lesions because it’s labor intensive and requires nursing expertise. Or, ask your doctor about learning how to do this technique at home.
• Light therapy.This treatment is used for people who either don’t get better with topical treatments or who rapidly flare again after treatment. The simplest form of light therapy (phototherapy) involves exposing the skin to controlled amounts of natural sunlight. Other forms use artificial ultraviolet A (UVA) and narrow band ultraviolet B (UVB) either alone or with medications.
• Though effective, long-term light therapy has harmful effects, including premature skin aging and an increased risk of skin cancer. For these reasons, phototherapy is less commonly used in young children and not given to infants.
• Talking with a therapist or other counselor may help people who are embarrassed or frustrated by their skin condition.
• Relaxation, behavior modification and biofeedback.These approaches may help people who scratch habitually.

DISEASE PREVENTION AND OCCUPATIONAL ADVICE ^[2]

• There is excitement about the possibility that atopic dermatitis and other atopic diseases may be prevented by altering the fetal or the newborn’s antigenic exposure. However, precisely what and when changes need to be made is not clear. There are conflicting data about whether maternal avoidance of milk, eggs and other dietary allergens during pregnancy and lactation can reduce the incidence of atopic disorders, but a Cochrane review of the evidence concluded that avoidance of such allergens in pregnancy protects the baby against the development of atopic dermatitis, and the same approach during lactation may have a small beneficial effect.
• The evidence that breastfeeding or diets to avoid potential allergens during the first 6 months of the infant’s life will significantly protect against atopy or reduce its manifestations is also contradictory. Although a cohort study of 1265 children followed for 10 years suggests that a diverse solid-food diet during the first 4 months of life roughly doubles the risk of developing atopic dermatitis, an American Academy of Dermatology guidelines task force review found that definite evidence for exclusive breastfeeding and dietary allergen avoidance was still lacking.
• There are suggestions that the use of hydrolysed infant formulas may be helpful, although perhaps not practical, for the prevention of atopic dermatitis in at-risk newborns. The use of probiotics, prebiotics or synbiotics as dietary supplements is also controversial.
• Atopic dermatitis will often improve about the time of puberty. This is often the time when adolescents are deciding what occupation they should undertake. Exposure of the skin to irritant chemicals and physical trauma should be avoided as far as possible. Adolescents with atopic dermatitis, particularly with hand involvement, would be well advised to avoid occupations involving wet work or exposure to irritants, such as car mechanics, engineering, hairdressing or nursing.

MIASMATIC APPROACH ^[5]

• PSORA
• Itching without pus or discharge
• Skin appears dirty, dry and harsh and becomes more dry with washing. The skin cannot endure water and often has an unwashed, unhealthy, dingy look.
• Rough skin.
• Crusts, which are thin, light, fine and small are present
• Small, sensitive, painful, non-suppurating boils, which may shed scrufy scales.
• Scanty, sour smelling sweat, especially on forehead and during sleep.

• SYCOSIS
• Exfoliating eczemas.
• Small, reddish, flat vesicular eruptions which are slow to heal.
• Acne, which is red in appearance.
• Skin looks oily appearance and perspiration is thick and copious.

• SYPHILITIC
• Threatening(ulcerative and destructive) appearance.
• Copper or raw ham coloured eruptions.
• Putridity and offensiveness of all discharges with ugly looking ulcers, which have a cadaverous base.
• All eruptions are patchy.
• Crusts are always thick.
• Offensive sweat.

• TUBERCULAR
• Skin conditions are angry looking and often accompanied by oozing of blood.
• Lesions are red and haemorrhagic in appearance.
• Eczema and ringworm, a history of ringworm and suppression of ringworm are tubercular.

REPERTORIAL APPROACH

KENT REPERTORY ^[6]

• CHAPTER: SKIN
• RUBRIC: ERUPTIONS
• SUB RUBRIC: ECZEMA
• ARS; ARS.I; CALC; CALC.S; CIC; CROT.T; DULC; GRAPH; HEP; JUG.C; JUG.R; LAP.M; MEZ; OLND; PETR; PSOR; TOX; SULPH; SUL.I

BOERICKE’S REPERTORY ^[7]

• CHAPTER: SKIN
• RUBRIC: ECZEMA
• AETHIOPS; ANAC; ANT.C; ARS; BERB.V; BOV; CALC; CANTH; CARB.AC; CIC; CLEM; CROT.T; GRAPH; HEP; KALI.ARS; MANG.AC; MERC.C; MERC.S; MEZ; OLEAND; PETROL; PLUMB; PSOR; RHUS.T; SUL; SUL.IOD; VINCA.

MURPHY’S REPERTORY ^[8]

• CHAPTER: SKIN
• RUBRIC: ECZEMA
• ARS; ARS-I; BAR-M; CALC; CALC-S; CIC; CROT-T; DULC; GRAPH; HEP; JUG-C; JUG-R; LAPPA-M; MEZ; OLND; PETR; PSOR; RHUS-TOX; SUL; SUL-I

HOMOEOPATHIC MANAGEMENT ^[9]

• SULPHUR
• HOT PATIENT
• TRIO BURNING
• When well selected remedies fail to act
• Complaints that relapse
• Offensive nature of discharges and exhalations
• SKIN: Dry, scaly, unhealthy; every little injury suppurates; Itching, burning ; worse scratching and washing; Pimply eruptions, pustules and; skin affections after local medical application.
• GRAPHITES
• CHILLY PATIENT
• Fat
• constipated
• Menopausal
• Sticky discharge
• SKIN: Rough hard, persistent dryness of portions of skin unaffected by eczema. Eruptions oozing out a sticky exudation. Rawness in bends of limbs, groins, neck, behind ears; Modalities: worse warmth, at night, during and after menses; better dark ,wrapping up.

• ARSENICUM ALBUM
• Trio burning
• Chilly patient
• Restlessness
• Prostration
• SKIN: itching, burning. Eruptions popular, dry, sclay, rough, worse cold and scratching. Better by warmth
• HEPAR SULPH
• Chilly patient
• Sensitive to cold and touch
• Every little injury suppurates
• SKIN: papules prone to suppurate and extend; unhealthy skin; chapped skin with deep cracks on hands and feet; sweats day and without relief; cold sores very sensitive. Cannot bear to be uncovered. Worse at dry cold winds, cool air, slightest draught, touch. Better by damp weather, from wrapping head, warmth.

• PSORINUM
• Chilly patient
• When well selected remedies fail to act filthy smell
• Sensitive to cold air or change of weather
• SKIN: dry, scaly eruptions disappear in summer retur in winter. Abnormal tendency to receive skin diseases. Dry, inactive, dirty look as if never washed. Coarse, greasy, as if bathed in oil. Suppression by sulphur sand zinc ointments.

• PETROLEUM
• Painful sensitiveness of skin of whole body; slight injury suppurates;
• Skin of hands rough and cracked; tips of fingers rough, cracked, fissured, every winter
• Tenderness of feet bathed in foul- smelling sweat
• CALCAREA CARBONICUM
• Chilly patient
• Fair, fat, flabby
• Increased perspiration
• SKIN: unhealthy, petechial eruptions; chilblains; nettle rash; better in cold air
• OLEANDER
• Itching scurfing pimples; nocturnal burning; very sensitive skin; slightest friction causes soreness and chapping
• Violent itching eruption, bleeding, oozing;
• Pruritis of scalp
• Want of perspiration

• VINCA MINOR
• Eczema of head and face. Oozing badly smelling moisture, matting the hair

• RANANCULOUS BULBOSUS
• Eczema with thickening of the skin and formation of hard honey crust
• THUJA
• Eczema worse after vaccination
• Skin extremely sensitive to touch
• Eruption only on covered parts < washing

• SILICEA
• Itching burning eruption < scratching, < covering warmly
• SARSAPARILLA
• Itching eruption on forehead and face like milk crusts with burning, becoming humid on scratching
• Base of eruption is much inflamed, child cries much. Crusts become detached in open air
• MERCURIUS
• Humid fetid eruptions, thick yellow discharge or yellow crusts on scalp surrounded by an inflamed border
• Itching< night, from heat of bed, sometimes attended by burning on scratching

• ANTIMONIUM CRUDUM
• Eczema with thick, hard, honey colored scales with oozing of green sanious pus which irritates the surrounding parts and burn and itch violently
• < bathing or working in water and at night
• Eczema capitis

• APIS MELLIFICA
• The eruption is moist, offensive and suppurating at times impetiginous
• Burning stinging pain. A red line marks the spread of the disease

• NITRIC ACID
• Humid stinging eruptions, bleeding easily when scratched
• NATRUM MURIATICUM
• Scaly eruption on flexor surfaces, bends of joints and folds of skin generally
• White scaly scabs on the head from ear to ear.
• Borders and corners of the eyelids raw and ulcerated oozing a corroding gluey fluid
• Has a particular affinity for the dorsa of the hand- the skin there becomes rough, dry and chapped
• SEPIA
• Peeling follows vesicles, which were not surrounded by very dry skin or it follows fine rash, worse about the joints or circular eruption like herpes circinatus
• Eruption during pregnancy and nursing
• Itching often changing to burning on scratching
• Eruption is dry or soon becomes moist and discharge copious offensive pus like fluid which becomes dry, cracks and exfoliate
• CLEMATIS
• More rawness. <washing
• Moist alternating with dry scabs

REFERENCES

1. CALVIN O. MCCALL, THOMAS J. LAWLEY. ECZEMA, PSORIASIS, CUTANEOUS INFECTIONS, ACNE, AND OTHE COMMON SKIN DISORDERS. HARRISON’S PRINCIPLES OF INTERNAL MEDICINE. 16^TH EDITION, MC GRAW-HILL, MEDICAL PUBLISHING DIVISION.
2. S. FRIEDMANN, M. R. ANDREN- JONES & C. A. HOLDEN. ATOPIC DERMATITIS, ROOK’S TEXTBOOK OF DERMATOLOGY (VOLUME: 1). 8^TH EDITION, EDITED BY: TONY BURNS, STEPHEN BREATHNACH, NEIL COX, CHRISTOPHER GRIFFITHS. WILEY-BLACKWELL, A JOHN WILEY & SONS, LTD., PUBLICATION.
3. DAVIDSON’S PRINCIPLE AND PRACTICE OF MEDICINE. 19^TH EDITION, PUBLISHER: EDINBURGH; NEW YORK: CHURCHILL LIVINGSTONE, 1995.
4. https://www.mayoclinic.org/diseases-conditions/atopic-dermatitis-eczema/diagnosis-treatment/drc-20353279
5. SUBRATA KUMAR BANERJEA, MIASMATIC PRESCRIBING. . 2^ND EXTENDED EDITION. PUBLISHED BY B. JAIN PUBLISHERS (P) LTD
6. T. KENT, EDITED AND REVISED BY CLARA LOUISE KENT, M. D., REPERTORY OF THE HOMOEOPATHIC MATERIA MEDICA. REPRINTED FROM 6^TH AMERICAN EDITION. PUBLISHED BY B. JAIN PUBLISHERS (P) LTD.
7. OSCAR EUGENE BOERICKE M. D. POCKET MANUAL OF HOMOEOPATHIC MATERIA MEDICA & REPERTORY, PUBLISHED BY B. JAIN PUBLISHERS (P) LTD.
8. ROBIN MURPHY, HOMOEOPATHIC MEDICAL REPERTORY A MODERN ALPHABETICAL AND PRACTICAL REPERTORY. 3^RD REVISED EDITION. PUBLISHED BY B. JAIN PUBLISHERS (P) LTD.
9. WILLIAM BOERICKE M. D. POCKET MANUAL OF HOMOEOPATHIC MATERIA MEDICA & REPERTORY. PUBLISHED BY B. JAIN PUBLISHERS (P) LTD.