THE epidermal cells are normally protected from damage by the tightly packed squames of keratin of the horny layer. The elasticity of keratin varies with its water content which can be reduced by evaporation or by removal of the lipid with which it retains moisture. Substances which produce inflammation of the epidermis (dermatitis) by mechanical or chemical disruption of the horny layer are called irritants. Degreasing agents such as soaps, if used repeatedly over a short time will cause dryness, redness, Assuring and irritation of the skin in almost everyone.
This traumatic or irritant dermatitis which accounts for four-fifths of dermatitis in industry is not dependent on hypersensitivity or allergic reaction, although there is considerable individual variation in susceptibility. The liability to such dermatitis will be increased in those who inherit an unduly dry skin or in later life when the activity of the sebaceous glands declines. Thus in old age, skin irritation may result from washing habits which in earlier life were harmless. Normally the skin has considerable powers of neutralising alkali but this buffering power is diminished in irritant dermatitis and as a result the epidermis is more prone to damage by alkalis. The skin is also more vulnerable after childbirth, a time when external trauma from washing infants’ clothing is also increased.
Dermatitis or eczema
A more violent skin reaction, contact or sensitisation dermatitis may befall the epidermis. The epidermal cells swell and disrupt, producing a sequence of changes which appear as erythema, swelling, vesiculation and exudation. This sequence of events, in particular the vesicular element is termed an eczematous reaction and the confusion of terminology between dermatitis and eczema has bedevilled dermatology for years. Eczema is a syndrome not a disease and can be caused by agents which reach the skin from from the outside surface, from the blood, or by an inherent instability of the epidermal cells present since birth or acquired later in life.
It has been conventional in England to call eczematous reactions produced from outside contact dermatitis and those eruptions due to endogenous or intrinsic factors, eczema. This arrangement has the merit of simplicity and will be used henceforth.
Acute contact dermatitis. (Dermatitis venenata—Sensitisation dermatitis)
Pathogenesis. Contact dermatitis is the result of an acquired sensitivity to substances which reach the skin from outside the body. The sensitiser penetrates the epidermis through the horny layer and via sweat ducts and hair follicles or trivial breaks in the keratin. There it combines with protein to form a stable antigen. This then sensitises lymphocytes giving rise to a specific cell-mediated capacity to react; any further contact with the sensitiser will be followed by an explosive inflammatory reaction of the epidermis which is mediated by the T lymphocytes and their effects on other cells. Immunologically this type of cell mediated reaction is classified as type IV delayed hypersensitivity.
There is always a latent interval between first handling a sensitiser and the development of sensitisation. This may be as short as 5 days but is usually months or years. At the time of sensitisation the whole skin of the individual becomes sensitised and experimental evidence has shown that this general sensitisation is carried on the T lymphocytes. There is no humoral antibody in the serum such as is found in Type I sensitivity, the anaphylactic reaction.
Patch testing, which consists in the application of a small amount of a suspected sensitiser to an area of apparently normal skin, depends on the spread of skin sensitivity. If the test is positive, an area of dermatitis will appear beneath the patch in 24—48 hours. Because of this, contact dermatitis is sometimes called the delayed allergic reaction. If no further contact with the sensitiser occurs, there is a gradual lessening of the sensitivity but in some cases it is lifelong.
Although there is hardly any substance, animal, vegetable or mineral, which cannot cause epidermal sensitivity, the capacity to sensitise varies greatly. Some substances such as the metals, nickel and chrome produce dermatitis, in a high percentage of those who handle them. An ability to form rapid protein bonds increases the power to sensitise, a capacity of the dyes like paraphenylenediamine and the chemicals used in the manufacture of rubber which are common offenders.
Just as the ability of substances to sensitise varies, so the ease with which an individual can be sensitised also varies. Contact dermatitis is rare before puberty and though difficult to prove statistically, it seems to occur more often in emotional crises. A person who has reacted to one substance is more likely to develop reactions to other materials even if chemically unrelated.
Cross sensitisation. Sensitivities are usually specific but sometimes the body cannot distinguish between chemicals of closely related structure. Thus a patient with a dermatitis due to hair dye (paraphenylenediamine) may also be sensitive to procaine and the sul- phonamide group of drugs. This phenomenon known as cross-sensitisation, may explain some of the sudden eczematous skin eruptions which arise after the first apparent contact with a material.
Clinical aspects of exogenous dermatitis. Although there is a theoretical distinction between dermatitis caused by irritants and true sensitisation, it may not be possible to separate the factors in an individual case. For instance, detergents remove lipid from the keratin thus allowing it to dry excessively and to split. At this stage the skin is rough and fissured, the change of a mild primary irritant dermatitis. The epidermal cells are now more easily damaged, since there is no longer a waterpoof intact horny layer, and sensitisation of the exposed skin cells can occur as shown by an increase in the inflammatory reaction.
Although detergents have been taken as an example, other degreasing agents damage the skin in a similar way; soluble oils and even cement also do so.
Another factor which plays a significant part is mechanical trauma. Lesions tend to occur where pressure or friction is greatest, i.e. on the axillary folds in clothing dermatitis.
When the problem of the cause of a skin eruption is posed, the first important question to answer is whether the eruption is a dermatitis due to exogenous contact and, secondly, can it be decided whether it is a irritant reaction or a specific hypersensitivity.
The clinical features of contact dermatitis are caused by violent inflammation of the epidermis and dermis. Where the skin is loosely attached, such as around the eyelids and on the scrotum, considerable oedematous swelling may simulate urticaria or even an acute cellulitis; but vesicle formation in the epidermis, to be followed later by weeping and desquamation, should indicate dermatitis. Although the diagnosis of sensitisation dermatitis is not difficult, the identification of the sensitiser calls for detective ability.
The history is of vital importance. One is entirely dependent on the accuracy of a patient’s memory for substances which have been handled but above all else it is important to determine the site of onset of the eruption since this will give a lead to the probable cause. A band of erythema around the forehead will of necessity suggest a hatband as the likely offender but contact dermatitis of the scalp caused by a hair dressing or dye will affect the skin of the forehead, ears and eyelids and may spare the scalp since this is remarkably resistant to irritants of all kinds.
The eyelids are susceptible indicators of sensitivity and may be involved in dermatitis from dusts, vapours and cosmetics. An uncommon catch for the unwary is the dermatitis of eyelids produced by nail varnish. Since the varnish is applied to the inert nail-plate no change can be seen on the fingers but isolated areas on the side of the neck and lids may be involved by occasional contact with the varnished nails.
Face powder, cream, rouge and lipstick all can produce dermatitis limited to the face and do not be misled by the patient who stoutly maintains that she has used the same brand for years. She may have taken years to become sensitive, or, a point that is often overlooked, the makers may have altered the constituents. Chemicals which may be light sensitisers are often added to soap and toilet preparations. Such photosensitive eruptions affect the face, V of the neck and the exposed parts of the limbs.
A knowledge of the habits of men and women is necessary to pose the right questions. Dermatitis behind the ears due to nylon hair-nets worn at night and dermatitis of the cheeks due to rubber sponges used for applying liquid make-up, are two examples which require some inside knowledge to elicit the cause.
Sensitivity to various articles of clothing can be diagnosed by the characteristic pattern of involvement. Ties produce a localised area at the front of the neck and beneath the chin. Shirts involve the axillary folds, the sides of the neck and the buttocks and thighs in those who wear their shirts beneath their pants.
The axillary lesions affect only the anterior and posterior folds, sparing the apex which does not touch the clothing. This is a useful differential diagnostic point, since the endogenous eruptions of psoriasis and seborrhoeic eczema involve the whole axilla.
Do not forget that dyes are not the only possible offenders in clothing. Formalin used in some drip-dry clothing, and other chemical finishes and even the man-made fibres themselves which may be colourless, can cause dermatitis.
A regional grouping of likely causes can be made—
Scalp. Hair dyes, brilliantines and scalp lotions.
Ears. May be involved by scalp applications, but also hair-nets, spectacle frames, ear clips, hearing aids and ear drops.
Eyelids and face. Plant sensitivity, airborne dusts, volatile chemicals, toothpastes, cosmetics, soap and nail varnish.
Neck. Ties, scarves, furs, necklaces (particularly the nickel and chrome clasps), nail varnish (from the habit of resting the chin in the hand), perfume.
Axillae. Clothing, rubber arm shields, deodorants, antiperspirants.
Trunk. Clothing, rubber and synthetic elastic undergarments.
Perianal region. Local application and toilet papers, lavatory seat.
Genitals. Dusts, clothing, contraceptives.
Thighs. Suspenders, either nickel or chromium and rubber, articles carried in pockets, matchboxes, chrome-plated objects.
Ankles and feet. Socks, stockings, rubber and metal foot supports, chemical dusts, rubber boots and shoes, dyes and adhesives used in shoe manufacture.
Hands and forearms, innumerable materials handled at work or in the house (liquids will tend to affect the finger webs and backs of the fingers and hands rather than the palms), plant sensitivity, rubber gloves and finger stalls, (palmar lesions are rare, but may occur from gripping tool handles, car gear levers, plastic, or rubber cycle grips, racket and club handles.)
Though a wide range of plants can produce contact dermatitis the common cause in Britain is primula obconica, the indoor primula. This causes a violent vesicular eruption on the fingers and forearms with the usual linear distribution of plant reactions due to contact with the leaves, and an urticarial swelling of the face and neck. This curious mixture of urticaria and dermatitis is not seen in other plant reactions. Even the papulo-vesicular lesions are a little unusual, often purplish in colour when they may be mistaken for lichen planus. Patients can be reassured that they can handle other varieties of primula safely, particularly the outdoor ones as these do not sensitise commonly nor cross- sensitise with primula obconica.
Dermatitis from other plants such as chrysanthemums, the next most common cause, is a less violent eruption which because of the redness and lichenification on the face and hands resembles atopic eczema.
A rare source of severe blistering on the exposed skin is contact with a plant which produces photosensitivity and this explanation should be suspected in agricultural workers (from handling parsnips) and picnickers who may lie on the stinking mayweed (anthemis) or gardeners cutting down the giant hogweed.
Medicaments applied to the skin are a common cause of sensitisation dermatitis and almost every application is capable of sensitising someone. A trivial abrasion can be converted into a violent weeping dermatitis by the use of a household antiseptic. Eyedrops, eardrops, rubbing oils, plasters are all potential causes of dermatitis. In a survey of over 100 proven examples of dermatitis caused by medicaments, antibiotics, local anaesthetic ointments and locally applied antihistamine preparations were the most common’offenders. There is in our opinion no justification for the use of penicillin, sulphonamides, chloramphenicol, benzocaine and the other ‘cain’ anaesthetics or an-tihistamines as local applications. Neomycin has been widely condemned as a common cause of dermatitis but it has been used more extensively than most other antibiotics and in our view the danger has possibly been exaggerated. The ointment bases including lanolin and the antiseptics (parabens) used to prevent bacterial contamination of ointments may cause sensitisation. Such a happening can explain aggravation of skin disorders by topical steroid applications which should in theory lessen inflammation. Sensitivities to medicaments arise most frequently around varicose dermatitis and leg ulcers, probably because of the long continued duration of treatment in these areas.
Confirmation of the exact cause of dermatitis can often be made by patch tests. We prefer to narrow the list of suspected substances by careful history taking and then to carry out selective patch tests. Only if these are all negative is a battery of common sensitisers applied.
However, the international contact research group test every patient with a battery of some 20 test substances. This method may show positive reactions which have not been suspected in the history. Some positive responses may not be relevant and there is also a risk of sensitising patients if this battery patch testing is repeated. This method does however give a good indication of the epidemiology of sensitisers.
Method of patch testing. Patch tests should not be performed whilst dermatitis is acute as this may be aggravated by the further slight contact with the sensitiser and false positive reactions obtained.
A small portion of the suspected material usually made up in a soft paraffin base is applied to an area of skin not involved by the dermatitis, usually the back or the inner aspect of the arm. If a fluid is being tested it is adsorbed on a square of gauze. This is then covered with cellophane or some other inert impermeable material. A ready prepared strip of aluminium foil such as A1 test is useful. The whole is held in position with adhesive tape. Control tests with similar materials should also be applied. If a patient is known to have a sensitivity to adhesive strapping the ‘patches’ can be held in position by proprietary tapes such as Blenderm. Dcrmicel or Micropore which are less irritant than the commonly used Elastopatches. The tests are left in position for 48 hours unless the discomfort of a violently positive reaction demands an earlier removal. A positive reaction consists of an area of inflammation beneath the suspected material which may vary from mild erythema to vesiculation or rarely necrosis. It is wise to wait 10 to 20 minutes after the patch has been removed since oedema may be suppressed by the pressure of the patch. If negative, the site of the patch should be inspected again 2 days later. Very mild positive reactions are slow in appearing. Care should be taken in interpreting results of tests. False positives may be due to using test materials which are in themselves primary irritants or, if the dermatitis is still active, a non specific false positive may be produced by the slight trauma of the test. A negative test does not exclude the substance as the cause of the dermatitis because the exact conditions under which it has been handled may not have been reproduced. Volatile substances such as perfumes which cause primary irritation under occlusion can be painted on the skin as an open patch test.
The international group recommends the following code for recording results.
Photocontact tests. When light sensitisers are to be tested a photopatch test is used. Paired patch tests are applied for 24 hours. Then one series of the test patches are removed and the areas irradiated with ultra-violet light. Photosensitivity is shown by a positive response 24-48 hours later on the irradiated test areas.
A usage test, i.e. further handling of the substance under natural conditions when the dermatitis has recovered may be the only way to prove the diagnosis if patch tests are negative.
Dissemination of contact dermatitis
After an area of contact dermatitis has existed for some time (the period may vary from days to months), extension to other parts of the body often occurs. This has been explained by the theory that some product of damaged skin, either alone or with bacteria, produces specific antibodies. Once these are present in sufficient amount, extension of the dermatitis to other areas of the skin will occur. This theory of auto-sensitisation is an attractive one, but as yet remains unproved.
There is a very definite pattern of spread from initial sites. For instance, lesions on the hands will first extend to the feet and vice versa. Lesions of the legs produce eruptions on the opposite leg and then on the forearms, face and neck.
Dermatitis of the scalp will involve the other hair areas, the axillae and groins.
Occasionally the signs of this secondary dermatitis are more obvious than the primary lesions.
Once this generalised spread has occurred, the skin remains in an excitable state. Any further skin damage, even years later, may precipitate a recurrence of generalised dermatitis.
Generalised exfoliative dermatitis
A rare sequel of extension of dermatitis is generalised exfoliative dermatitis (Erythroderma) and an almost identical clinical picture may be produced by extensive psoriasis. In this condition the whole of the patient’s skin becomes a dusky red, dry, scaling so profusely that a dustpan and brush may be required to sweep up the pile of scales shed when the patient removes his clothes. The skin over the whole body is oedematous and pits on pressure, while the legs are often grossly swollen. Lymph nodes in the axillae and groins are so enlarged that they become visible. In the elderly oedema of the face in the inelastic senile skin causes the eyelids to be everted (ectropion) and conjunctivitis results. There may be severe loss of hair and shedding of nails.
Blood flow to the skin, which as a whole is a very large organ, is so greatly increased that in an elderly patient on the verge of heart failure the strain on the heart may be sufficient to precipitate him into actual failure. The dilated blood vessels in the skin lose their power to contract, and thus lose their thermoregulatory function. Heat lost through the skin is so great that the patient can quickly take on the temperature of his surroundings and even in a centrally heated ward can develop a ‘ seriously subnormal temperature.
Finally, severe generalised disorder of the skin upsets the function of the gut causing malabsorption of fats, iron and vitamins and protein loss both from the gut and from the severe scaling of the skin. In those cases which occur without any history of previous skin disease it is important to exclude the possibility of an underlying Hodgkin’s disease or leukaemia. Thus biopsy of the skin, lymph gland and bone marrow may be necessary to attain the correct diagnosis.
Treatment of dermatitis
Identification and removal of the exciting cause is the first step in treatment. The nature of the disorder should be explained since fear and anxiety aggravate symptoms and most patients associate skin disease with dirt and infection. It is also important to explain how to avoid further contact with possible sensitisers. It has been shown that a complete avoidance of contact with substances such as nickel may in fact in time lessen the degree of sensitivity.
Treatment of irritant dermatitis. Protection against further contact with irritants such as soap and water in the case of the housewife, can only be obtained by the wearing of cotton gloves beneath P.V.C. gloves. Dry housework can be done in cotton gloves and the presence of the gloves is a reminder to put impermeable gloves on when about to do wet work. Lined impermeable gloves are not so satisfactory. The local treatment of irritant and contact dermatitis is essentially the same. A simple emollient such as aqueous cream BP is all that is needed in the mild case.
In more severe cases, applications of one of the anti-inflammatory topical corticosteroids is now the usual first choice. Other non-steroid anti-inflammatory creams have not as yet proved their worth. Corticosteroids are prescribable in a variety of vehicles, lotions, creams, ointments and aerosol sprays. There is no indication for the aerosol spray. The modern base contains the features of cream and ointment in being water soluble, and therapeutically there is nothing to choose between the cream and the ointment. Since they contain an anti-inflammatory steroid they can be applied directly to a moist surface and there is no necessity to use the traditional lotion. The medicament is applied sparingly with the tip of the fingers spreading it as far as possible. Adjacent surfaces should be separated by a layer of linen or gauze. No covering is needed for the face or scalp but patients may feel more comfortable if the limbs are covered by Tubegauze and the hands by cotton gloves.
The range of steroids seem”, limitless but they all reduce erythema, oedema and exudation, and in the treatment of acute dermatitis, hydrocortisone, the first to be introduced, is almost as effective as the most modern and actively penetrating preparation.
The disadvantage of the powerful steroids in their standard strength is their ability to damage the collagen of the dermis, producing atrophy. They should therefore be used as sparingly as possible, avoided completely on the face and also in the axillae and groins where telangiectases and striae may be quickly produced. They can be used effectively and safely in dilutions of up to 1 in 10 in a cream base provided the diluent is correct for the steroid. Some of the corticosteroid activity can be lost if an incompatible diluent is used. Applications should be repeated 6 to 8 times daily and reduced in frequency as the inflammation lessens. Sudden cessation of treatment should be avoided as a rebound acute recurrence of the dermatitis may follow. The corticosteroid applications must be gradually tailed off to once daily, alternate days and even twice weekly. It has been shown that a reservoir of steroid remains under the homy layer as long as a week and small amounts continue to be released to the underlying dermis. The indication for the use of powerful steroids at standard strength is in the treatment of hands and feet where the weaker preparations cannot penetrate the thick skin. If there is not speedy response then extra penetration can be obtained by occlusion for 8 hours nightly under elastic gloves or bags.
Normally no antiseptic or antibiotic need be combined with the steroid and, in fact, are better avoided as they may sensitise the already inflamed skin. For the same reason antihistamine preparations, in particular those mixed with calamine, should not be used. The only exception for combining an antiseptic effective against Candida with a steroid is when treating such areas as the perianal region or the external ear. Areas of dermatitis should not be washed with soap but should be cleaned with an emulsion of water and ung. emulsificans, liquid paraffin or olive oil.
Where secondary infection is obvious particularly in treating hands and feet, wet dressings of ¼ strength sodium hypochlorite solution dilute B.P.C. (Milton) are effective and infection should also be controlled by systemic antibiotics. Rest in bed lowers capillary pressure in both upper and lower limbs and will assist the control of persistent exudation.
Treatment of sub-acute and chronic dermatitis. When a dermatitis has persisted for some time the skin becomes thick, scaly and lichenified and the habit of scratching is deeply ingrained. The addition of an an-tipruritic such as coal tar to compound zinc paste may lessen skin damage and allow healing to occur. Often it may be necessary to use an occlusive medicated bandage which can be applied directly to the skin and kept in position for 7 days. These can be applied to fingers separately, held in position by Tubegauze, thus allowing a dry hand occupation to be continued. Bandages are impregnated with simple zinc paste, ichthyol paste, coal tar paste and even corticosteroids. Coal tar bandages have in our hands been most effective in chronic dermatitis. The great advantage of occlusion is that anxiety is lessened by hiding the lesions, experiments in self-treatment are impossible and injury from scratching is cut to a minimum.
Drugs. There is no specific internal remedy for dermatitis but in some cases there is an undoubted dermal component or urticarial element responsible for itching which can be controlled by antihistamine drugs. Since the majority of antihistamines also have a sedative effect this is also of benefit. Promethazine hydrochloride (Phenergan) 25-50 mg at night is effective. A good night’s sleep is vitally important and of the sedatives dichloralphenazone (Welldorm) or nitrazepam (Mogadon) are safe. The use of any drug should be considered carefully in the very old as antihistamines can cause retention of urine, and mental confusion is easy to produce even with nitrazepam.
The temptation to use systemic corticosteroids in widespread dermatitis should be resisted in all but the very worst situations for although symptoms may be suppressed by corticosteroids there is often considerable difficulty in the withdrawal of treatment without recurrence of the eruption. Should the decision be made to use corticosteroids then prednisolone 10 mg three times a day is a standard starting dosage, which should be lowered as soon as the skin shows improvement.
Treatment of exfoliative dermatitis. One absolute indication for the use of corticosteroids would be the onset of exfoliative dermatitis where a dose of 30-60 mg prednisolone daily may be necessary. Two special precautions are required in the management of this condition. The temperature of the patient should be taken with a special low reading thermometer as subnormal temperatures can easily pass unrecognised. They should also be nursed in isolation as the scales of keratin which are released in large numbers carry pathogenic organisms which may infect other patients. A room in which the temperature can be regulated is ideal.
The possible diagnosis of light sensitisation of the skin should arise if an erythematous or vesicular eruption appears on the areas of the face, neck and hands which are normally exposed to sunlight. The parts involved resemble those affected in a dust dermatitis but light eruptions spare the eyelids, the upper lip and the neck under the chin as all these regions are in shadow. A helpful point in the history will be the seasonal variation; in Britain most light eruptions begin in the spring—March or April—and clear at the end of September.
Light reactions have been divided into phototoxic in which there is an exaggerated sunburn response which soon passes off and photoallergic which once induced may persist for years.
The causes of photosensitive reactions are similar to the causes of any eczematous eruption. Thus photosensitivity can occur from external contact sensitisers, from drugs and metabolites and as a spon-taneous disorder comparable to constitutional eczema. Eosin in lipstick, perfumes in cosmetics and pitch and tar fumes are well known contact light sensitisers and in recent years a germicide added to a popular soap produced an ‘epidemic’ of photosensitisation. Most chemical causes of light eruptions are themselves ‘fluorescent’.
A very wide range of drugs produce light sensitivity and the possibility should be considered in any light eruption. Of those in popular use the phenothiazines, sulphonamides, chlorothiazides and demethyl chlortetracycline head the list. Some produce light sensitivity when used as local medicaments as well as when taken internally. Confirmation of the diagnosis can be obtained by photo-patch testing.
Polymorphic light eruptions
In many light eruptions a sensitising chemical either of exogenous or endogenous origin c innot be found. Such eruptions may appear rarely as bullae on the face in childhood and more commonly as a papular eruption on the upper margin of the ears in early spring. In adults an idiopathic light eruption often starts after severe sunburn. The following spring an irritable eruption of papules, plaques and vesicles appears and persists throughout the summer months. Often this will recur year after year in the same month, clearing in the autumn. There may be difficulty in differentiating such eruptions from discoid lupus erythematosus or from disseminated lupus erythematosus, and an apparently benign light eruption may after some years show the biochemical change of lupus erythematosus. It is most important therefore that idiopathic light eruption be investigated thoroughly to exclude both lupus erythematosus or porphyria which can also produce light sensitivity.
Sometimes injury to the skin by ultra-violet light may produce a Koebner phenomenon and then disorders such as psoriasis and atopic eczema may be more evident on the light exposed areas.
In the elderly, chronic eczema tends to involve the face and hands and at times becomes infiltrated and papular. Histologically this infiltrated light damaged skin resembles a reticulosis, and the syndrome has been termed actinic reticuloid.
Nowadays more sophisticated apparatus is available for the investigation of light eruptions and it is possible to analyse the wavelength of the light which damages the skin, the action spectrum. Thus the sunburn range is in the region of 290 to 320 nm but visible light extends to 400 nm and over. It is known that actinic reticuloid is made worse by rays in the visible range and it can therefore be aggravated by light which passes through window glass and even by fluorescent light tubes in the house. The reaction in porphyria also occurs with visible rather than short wave ultra-violet light. Thus determination of the wavelength of the light responsible for a dermatosis may be a very useful clue in the diagnosis of the etiology.
Treatment. The immediate treatment is that of any dermatitis. The skin may be protected against further exposure by applying creams which either prevent the passage of light rays by their content of opaque powder such as titanium dioxide or by their ability to absorb the wavelength which damages the skin. Mexenone (Uvistat) is a popular and effective light-absorbent cream against sunburn. It can be combined if necessary with an opaque powder if it is not effective alone. Another effective sunscreen is Paraaminobenzoic acid dissolved in 70 per cent ethanol (Spectraban). This has the added advantage of being non-greasy. Neither of these creams, however, will protect patients who are sensitive to visible light.
Antimalarial drugs, such as chloroquin sulphate 200 mg daily, do alleviate some cases of light sensitivity but in view of their side effects, should be used for only very short periods such as-the 2 to 3 weeks of a summer holiday. There remain a number of sufferers from light sensitivity who cannot be relieved by medicaments and for them shady hats, long sleeves and gloves remain an uncomfortable solution. It may even be necessary to keep them indoors behind windows covered with a filter which will only permit long wave length light to pass through.