The oral use of cortisone has a place in the treatment of eczema in infants and children, but I do not think such an important place as it has in asthma. I have treated about sixty eczematous children with it, and have come to some fairly definite conclusions about it. In the first place, it is not a cure, and not infre­quently when it is discontinued, the eczema returns and is worse and harder to get rid of than it was be­fore. This is particularly true if it is used in patients where there is a bacterial element to the eczema, as there is in atopic erythroderma and infectious eczematoid dermatitis. I have come to the conclusion that it is best not to use it for atopic erythro­derma, unless just for a few days to tide over some very difficult situation.

The reason for this is that in atopic erythroderma it is necessary to use too large doses and to continue it over too long a period of time. When it is discontinued, the whole trouble is likely to recur worse than it was before and may be harder to get rid of, so that the duration of the eczema may be actually increased rather than lessened by the use of cortisone. I expect that the reason probably is that bacterial growth is encouraged rather than inhibited. I do not ad­vise its use for a baby who has blue feet with or without erythroderma, or for nummular eczema.

I have found these things out by bitter experience. It ought not to be used if the eczema can be reasonably well controlled in other ways. It is, however, of very considerable value in certain situa­tions. I have had several babies with oozy, crusted faces, which were kept inflamed by rubbing to such an extent that the usual methods of treatment were of no value. The oozing and itching were promptly controlled with cortisone, and did not recur to any great extent when it was discon­tinued.

Pig.   37.-Before  cortisone treatment.     (From New   England  J.  Med.,   1953.)
Fig.   38.-After one  week  of  cortisone  treat­ment.   (From New England J. Med., 1953.)

Another type of patient for whom cortisone is often satisfactory is the child of 3 to 5 years with a diffuse deep-seated papular eruption all over. Cortisone will usually re­lieve this quite promptly and give you and the patient a breathing spell, and a chance perhaps to find the cause of the eczema, which is often some specific food in this type of eruption.

Another indication is in the older child whose eczema is just so terrible that nothing can be done with it. He has been to a number of different doctors, has been dieted, innumerable salves have been used, and still he is no better. He is awake most of the night, and so is his mother, so that a very bad situation has developed in

the family. They all are worn out, and irritable, and immediate relief of the situation is necessary. Still an­other situation where cortisone is of value is in severe atopic dermatitis due to pollen, as in pollen eczema it is not necessary to continue the corti­sone very long.

I have made it a rule never to give more than 75 mg. of cortisone a day to an infant or young child with eczema; if they need more than this I do not want to treat them with cortisone. I usually start with this amount, and in a few days when the eczema is controlled, as it usually is, drop the dose to 67.5 mg. a day for a few days, then to 50 mg., and finally to 37.5 mg. There are few patients with eczema who get any benefit from a dose smaller than this. To the babies under 2 years I have given 5 grains of potassium chloride daily; for older children I have simply pro­hibited the use of added salt to the food after it has been brought to the table. I have usually had the mother call me by telephone three days after the cortisone was started, have seen the child a week after it was started, and from then on every two to four weeks according to circumstances. I do not try to get rid of the eczema entirely, lout simply to keep it under reasonably good control, as this can usually be done with moderate doses. It seems to me that the use of large doses is not justified in such a disease as eczema, because the trouble that may arise from large doses may be worse than the original disease.

There is a rumor around that corti­sone stops the growth of children. As I write (April, 1955), nothing to my knowledge has as yet been published about this. I have kept growth rec­ords in the last three years of forty-three allergic children who have been treated with cortisone for periods varying from three months to three years. There were 417 months of cortisone treatment.

Fig. 39.-Cushing’s syndrome, produced by only 50 mg. of cortisone a day. This is very unusual. (Prom New England J. Med., 1953.)

During this time these children gained 80.75 inches in height. Forty-three normal chil­dren of the same age, height, sex, and percentile height group would have gained in the same time 86.25 inches. This is a difference of only about 7 per cent. These figures have been examined by two expert statisticians and they reached the conclusion that from them it could not be concluded that the use of cortisone retarded growth, nor could it be concluded that it did not retard growth. It is clear, however, that if growth is retarded it is not retarded enough to amount to anything, which after all is what we want to know, and no child who needs cortisone should have it withheld for fear that it will dwarf him – it will not.

My favorite preparations are as fol­lows :

Crude Coal Tar Undiluted.-This is not used enough; people have for­gotten about it, but it should be re­membered that when coal tar was first introduced in Switzerland and in France about 1910, it was always used in this way. Its incorporation into ointments came later. Undiluted tar is used on small thickened areas any­where on the body. It is painted on twice a day, and dusted over with tal­cum powder. It is very useful for the small cracks at the lobes of the ears, which are so common in atopic dermatitis.

Tar Pastes and Ointments.-These, of various strengths and made with various vehicles, are unrivalled in the local treatment of eczema in infants and children. Sensitization is un­usual. It is best not to use a tar preparation on a hairy area, or where there is any pustulation. Tar is photosensitive and should not be used on the face if there is to be exposure to bright sunlight or considerable irritation may result. The mother should be told of this. The more chronic and thickened the eczema is, the stronger the tar preparation should be. I have never seen any bad results from absorption, but have heard of them, and it should be re­membered that tar is a complex sub­stance, containing elements which are toxic if absorbed in large amounts. I have followed the rule not to use a tar preparation over a very large surface area, and have limited its use at one time to both legs, both arms and the face, or to the trunk.

My favorite preparations are the following:

(1)  Crude  coal tar 3  i Zinc oxide 3 ii Starch 3 iv Petroleum jelly % ii

This is about 5 per cent strength, and is the original tar paste used by Dr. Charles J. White, as he intro­duced it at the Massachusetts General Hospital in 1912. It is black and dirty.

(2)  Crude coal tar

Yellow wax aa 3 i ss Petroleum jelly Lanolin aa ad 3 ii

This is sometimes used on very thick chronic places (ankles or wrists), where there is no moisture, so a paste is not necessary, and it is desired to secure good penetration. It should not be simply spread on the skin, but well rubbed in. It is sometimes of advantage to add 10 grains of sali­cylic acid to the ounce. It is a strong-ointment-I use it only occasionally.

(3) “Daxalan”  ointment.*

This is similar in composition to No. 1, only a little weaker (3 per cent). It is a remarkably smooth and well-made preparation, and is pre­pared so much better than most druggists can make tar ointment that for a long time I have not used prescription No. 1, but have pre­scribed Daxalan instead. It is black and dirty.

(4)  Kolpix “A” and Kolpix “D.”

These ointments are also made by the Dome Chemical Company, and differ somewhat from the Daxalan ointment in that the tar has been treated in some way so that it is a medium gray color instead of black, and the base is not greasy but water-soluble. The strength of each is 2 per cent tar. Kolpix “A” is for acute, somewhat active eczema, Kol­pix “D” for chronic eruptions. Neither is very dirty. These are fine preparations-I use them a great deal.

(5) Tarquinor.t

This is another fine tar preparation, also in a water-soluble base, and not very dirty. Its strength is 1 per cent, and it has added to it 0.20 per cent of Quinolor, an antiseptic.

(6)  Tar and bentonite pastes.

At the Children’s Hospital about 1942, Mr. Donald Skauen, the hospital pharmacist at that time, in collabora­tion with friends at the Massachusetts College of Pharmacy, which is across the street, and with a few suggestions from me, developed a thick tar paste, which has proved very useful. It is made thick by bentonite, and smooth by adding a certain vanishing cream.

Fig. 35.-Ordinary atopic dermatitis. Local treatment: Daxalan ointment or Kolpix oint­ment A. It is a little too thick for hydro-cortisone ointment.

Pig. 36.-Deep papular form of atopic dermatitis. Local treatment: a 3 or 5 per cent tar paste. Hydrocortisone ointment does not do well for this type. (From New Eng­land J. Med., 1953.)

It can be made in various strengths, and we have called it Tar and Bentonite Paste Nos. 1, 2, and 3. The No. 1 is very weak, the tar in it being de­rived from liquor carbonis detergens (N.P.) ; the No. 2 contains 2 per cent of coal tar, the No. 3 contains 5 per cent. These pastes are much thicker than the other tar pastes and stay on the skin better. I use the No. 1 a great deal when I want a protective, rather mild, clean preparation for use on places that are not much thick­ened. There is too little tar in this preparation for it to be of any value in chronic, thickened eczema. It is not dirty. I use the No. 2 and No. 3 occasionally, but am more likely to use Daxalan or Kolpix.

Tar and Bentonite Paste No. 1

Bentonite    (TJ.S.P.)                                 7.50

Liquor carbonis detergens      (N.F.)           15.0

Water                                      15.0

Special vanishing cream or “Neo-
base” or Hydrophilic ointment
(U.S.P.)                                                   7.50

Paste zine oxide  (U.S.P.)                             45.0

For Paste No. 2, 2% of crude coal tar is used instead of the liquor carbonis detergens, and for Paste No. 3, 5% tar is used.

Special Vanishing Cream

Glyceryl monostearate                               8.0

Spermaceti                                                 7.0

Theobroma oil                                          5.0

Liquid petrolatum                                      8.0

Distilled water                                           67.0

Glycerin                                                    5.0

Methyl   parahydroxybenzoate                  0.0625

Propyl   parahydroxybenzoate                  0.0375

(7)  Hydrocortisone ointment  (1%, 2.5%)

This is a valuable addition to the armamentarium, although I am not quite so enthusiastic about it as some have been. I have treated, to date, about 120 infants and children with it. It is of most use for inflamed, rather superficial, slightly scaly areas. It does not do as well when there is no active inflammation and a good deal of thickening-for such places a tar preparation is better. It should be applied twice a day, and gently rubbed in.

The 1 per cent ointment in most cases works about as well as the 2.5 per cent and is much less ex­pensive. Hydrocortisone ointment is not a cure-it simply reduces inflam­mation, but it does this with remark­able efficiency. If it has worked well, and after a few days there is no more eczema, it is discontinued until the eczema returns, and then resumed. If after a while the 1 per cent oint­ment does no good, then the 2.5 per cent can be tried. If this does no good, go back to the older methods of treatment. Hydrocortisone oint­ment is by no means a cure-all for eczema, and there is still plenty of room left for the older preparations that have been successful for years in local treatment.

Some hydrocortisone ointments con­tain an antibiotic; some do not. It is best, if there is any question that the lesion being treated is infectious eczernatoid dermatitis, to use one of those that contains an antibiotic; several times I have seen such places develop gross infection after the use of the ointment without an antibiotic, and at least once when a hydrocorti­sone ointment containing neomycin was used. I think it best, if gross infection is present (pustulation), not to use hydrocortisone ointment either with or without added antibiotic, but to get rid of the infection by the means which have been previously described. So far as is known, no systemic effects are produced by hydrocortisone ointment.

The general character of the skin means a good deal so far as prognosis goes-if it is soft and smooth where there is no dermatitis, the prognosis is much better than if it is of the dead, dry, “asteotic” type. In some children with atopic dermatitis there is seen an exaggeration of the small crisscross lines, with or without thick­ening, that run across the palm of the hand. (See Fig. 32.) This indicates chronicity, and means, as a rule, that you are dealing with a stubborn and a difficult case.

(7) Swartz’s ointment:

Salicylic acid gr. xxx Mercurochrome  crystals gr. xx Aquae q.s. Anhydrous lanolin Petroleum jelly aa 3 i

Fig. 33.-Subacute atopic dermatitis.    Local treatment:     Swartz’s ointment.    It almost always does remarkably well for this type.     (Prom Brennemann’s  Practice  of  Pediatrics.)

This was originated by Dr. Jacob Swartz of Boston over thirty years ago for the. treatment of fungus in fection, for which it is still good. I happened to use it once on a child who had no fungus infection, but subacute atopic dermatitis in front of the elbows and back of the knees. It worked so well that I have used it constantly ever since for such pa­tients. I have never seen it irritate, and it almost always does good, for what reason I have no idea. It should be well rubbed into the skin and not simply spread on. If the dermatitis is thick and lichenified, a strong tar paste or ointment is better. (See Fig. 34.)

(8)  Vioform.

This is used as a 2 per cent oint­ment either in petroleum jelly or in hydrophilic ointment (U.S.P.), or as a paste in the same strength with paste zinc oxide (U.S.P.) as the base. It is a fairly good antiseptic and fungicidal agent, is usually well tolerated, and is not likely to sensi­tize. I have used it especially on the arms and legs of infants with atopic erythroderma, and sometimes for moniliasis of the abdomen and pubic region. It is a good preparation, but I think its value has been somewhat exaggerated.

(9)  Burow’s solution 3 i ss

Hydrophilic  ointment   (U.S.P.)   3  vi Paste zine oxide (U.S.P.)  I i

This is a soothing, slightly drying, excellent preparation for acute derma­titis if it is not too wet.

(10)  Lassar’s   paste    (paste   zinc   oxide, U.S.P.)

This is an old and tried preparation of value. It has the virtue that the large amount of starch it contains enables it to absorb a little fluid, and it is so thick that it is protective. I use it for acute angry eruptions in order to get them calmed down a bit before using tar, and as a protection, applied thickly with a throat stick, for ammonia dermatitis.

Fig. 34.-Lichenifled atopic dermatitis.    Local treatment:     a strong tar paste. (From Brennemann’s Practice of Pediatrics.)

(11)  Crude coal tar.

This is the most valuable local remedy there is for most infants and children with atopic dermatitis. It can be used as it comes, undiluted, or in pastes or ointments made up in various bases, and of various strengths.

Although sometimes much good is done by immunologic treatment, and it is certainly worth while because it attempts to get at the cause of the disease, too often it does not actually accomplish much. When all is said and done, skillful local treatment is more valuable than anything else.

It is not necessary to have at your com­mand a large number of preparations. The proper use of a few is more im­portant, and after you have treated many of these patients you begin to see what really works and what does not. It is important to bear in mind that at any given time the eczema may be in different stages on different parts of the body, and one part may need an entirely different treatment from another part. In general, mild

preparations are used for acute eczema, strong preparations for chronic. My favorite lotions, ointments, and pastes are as follows:

I. For Acute Oozing Eczema.- If there is much oozing, a clear wa­tery lotion should be used-not a shake lotion or a salve.

Fig. 29.-An oozy face which has been treated with a shake lotion. This should not be done. Proper treatment is with Burow’s solution, camomile tea, or potassium perman­ganate. (From Brennemann’s Practice of Pediatrics.)

It is best used as a continuous wet dressing, or if this is not possible, it should be sopped on very frequently.

(1) Burow’s    solution    1    tablespoonful Water 1 glassful

(2) Potassium permanganate 1 to 10,000 Potassium permanganate gr. vi Water g iv

1 teaspoonful to 1 quart of water gives about a 1 to 10,000 dilution of permanganate

or

A 5-grain tablet to a gallon of water gives about a 1 to 12,000 dilution

(3)  Silver nitrate  solution,  0.25%.

This  is  used  for  small   areas  only.

(4)  Camomile tea. This is prepared by steeping 4 teaspoonfuls of camomile flowers in a quart of boiling water for 20 minutes. Then strain.

II. Shake Lotions.-

There are innumerable shake lotions. I use the three below more than any others.

(1) Burow’s solution 3 iv Zinc oxide

Talc aa 3 i

Glycerin 3 vi

Lime water 3 iv

This is somewhat astringent and sooth­ing. It is useful for slightly moist areas where two skin surfaces come together as in the front of the neck, axillae, and groins.

(2)  Calamine lotion (TJ.S.P.) (without carbolic)

(3)  Liquor  carbonis  detergens   (N.F.) Glycerin aa 3 iii Calamine   lotion    (U.S.P.)    ad   5 vi

These lotions are useful for rather mild, extensive, maculopapular erup­tions on the trunk. If tar is tolerated No. 3 is better than No. 2. This lotion is painted on with a small ordi­nary paintbrush. If it is too drying it can be alternated with one of the mild “creams” listed below.

III. Ointments and Pastes.-

(1)  Acid Mantle Creme* ‘

(2)  Neobaset t

(3)  Hydrophilic    ointment (U.S.P.)

(4) Petroleum jelly

(5) Toilet lanolin*

None of these has any great thera­peutic action. They are used where the skin is dry, scaly, and where a mild soothing and lubricating action

*Dome Chemical Co.

t Burroughs Wellcome & Co. JE. R. Squibb Co.

Fig.  30.-Papular  form  of  diffuse  atopic  dermatitis.     Local  treatment:     calamine  lotion  with added   liquor  carboms  detergens.     (From   Brennemann’s   Practice   of   Pediatrics.)

Fig.   31-Pruriginous  form   of  atopic   dermatitis.     Local   treatment:     calamine   lotion   with liquor carbonis detergens. Lotions are better than salves for this type.
(From Brennemann’s Practice  of Pediatrics)

is desired. Many children over the age of ten years with long-standing atopic dermatitis have very definite ideas about what they like to use, and what their skin will tolerate. Most of them find that some mild soothing application, such as one of those above, give them as much relief as anything. The first three are water-soluble, the last two are not. Lanolin should not be used if there is sensitivity to wool. There is a great difference in what skins with long-standing atopic derma­titis can tolerate. For some, a greasy preparation such as Lanolin or petro­leum jelly may be irritating; for oth­ers these work better than the water-soluble ointments.

(6)  Salicylic acid gr. xx Petroleum jelly % ii

This is sometimes useful after Swartz’s ointment has been used and there are many small adherent shrivelled scales left on the skin.

Fig. 32.-Note thickening of palm and many flne crisscross lines. This appearance is seen in atopic dermatitis which has lasted a long time. It will continue to last a long time. Such an appearance of the palms is of rather bad prognostic import. (From Brennemann’s Prac­tice of Pediatrics.)

The use of this ointment softens them, and they can then be detached by washing with pHisoderm. Some older children with atopic dermatitis have very “dead,” dry, thick, scaly skins all over which closely approach ichthyosis. Many have keratosis pilaris, which consists of many little horny plugs in the follicles, and is seen particularly on the outer surface of the upper arms and on the lower legs.

Still others have “keratosis palmaris et plantaris,” which is often hereditary, and which is shown by great keratotic thickening of the palms and soles. These three condi­tions cannot be entirely cured and they complicate the therapeutic prob­lem, for such skins “eczematize” very easily from any sort of chronic ex­ternal irritation, particularly in the winter. Ointment No. 6 is helpful; it should not be used over a large body surface at one time. In most textbooks of dermatology large doses of vitamin A are recommended for ichthyotic skins and for keratosis pilaris. I have never seen it do any good.

Treatment.-The two most impor­tant things in treatment are to eradi­cate infection in so far as it can be done, and to keep the baby in as good general condition as possible by giving him plenty to eat. He is in for a long sickness, no matter what is done, and adequate nutrition is of great importance to enable him to weather it. These babies are the most highly allergic people there are; their degree of sensitivity to egg white is terrific, and every one of them that I have  been able to  follow has later developed asthma or hay fever. In years gone by I did fairly com­plete indirect testing on twenty-three of these babies.

Fig.   25,-Atopic  erythroderma  without scaling.     Local   treatment:     petroleum   jelly, washing with pHisoHex

Fig.   26,-Atopic  erythroderma with slight  scaling.     Note   enlarged  glands   in  groin   and   poor nutrition.

There were reagins to egg white in twenty-three, to wheat in nineteen, and to milk in ten, and occasionally  reagins  to   other  foods and to dust and feathers. Removal of foods or environmental allergens does little or no good- these patients do no better in a hos­pital than at home. I am sure, however, that if they ate egg white they would have violent symptoms, and it is best to give them no wheat.

Fig. 27.-Severe atopic   dermatitis,   changing  later  to  atopic   erythroderma.     Before   extensive scaling”.    Note normal skin in diaper area.     (From Brennemann’s Practice  of  Pediatrics.)

Fig 28 – Atopic erythroderma. Same patient as in Pig. 27, three weeks later. Local treatment: petroleum jelly with 5 grains of salicylic acid to the ounce. (Prom Brennemann’s Practice of Pediatrics.)

A milk-free food does them no good; in­deed it may do harm, for diarrhea is to be avoided at all costs. For over ten years I have done no skin testing either direct or indirect on these babies and am able to treat them better now than I did previously be­cause after a good deal of useless dietetic treatment I have come to realize that food sensitivity is not the main cause of their trouble. For some years I have given them the diet mentioned before, consisting of milk, rice or oat, lamb, banana, squash, string beans, carrots, apple sauce, and Vi-Penta drops. I think they do better on a formula with half the cream removed, and with 3 or 4 added tablespoonfuls of Casec to the quart, as discussed under Seborrheic Dermatitis. I have also thought that large doses of ascorbic acid (100 mg. a day) possibly did some good.

Reduction of the bacterial flora of the skin and the prevention of any localized pyogenic infection are of prime importance, and it is best to give moderate doses of some antibiotic right along. This, however, does not produce any striking results.

Local treatment likewise is directed at antisepsis of the skin. For the arms and legs I use 2 per cent Vio-form either in petrolatum or in zinc oxide paste, depending upon the con­dition of the skin, or a mild tar paste. For the face, the same, and for the trunk, a mild vanishing type cream or plain petrolatum. I like to have these babies washed twice a day with pHisoHex, which is a mild antiseptic and may do some good. An alternative to this method of treatment is to dip the baby twice a day in a bath of 1 to 10,000 potassium permanganate solution and let him stay there ten minutes. I have sometimes seen this do very well, particularly if there is a tendency to oozing.

I think these measures do some good, but progress is slow no matter what is done. These babies are never cured quickly. Toward the end of the second year they recover. One of the first signs of beginning recovery is that the feet are no longer blue and cold. Then the enlarged glands begin to go down, the erythroderma gradually lessens and white patches of skin begin to appear. It is my im­pression that they do not have atopic dermatitis later in childhood, but I have not enough accurate figures to be sure of this.

What I have called “atopic erythroderma” is atopic dermatitis, but it is a rather special form of atopic derma­titis, and warrants separate discussion. It may begin in a baby 3 or 4 months old, exactly as Leiner’s disease does, or it may develop from a severe and generalized atopic dermatitis. The skin is bright red all over, usually with extensive scaling. Vesiculation is not prominent. A marked general glandu­lar enlargement is one of the most characteristic features. These glands, particularly in the axillae, may be as large as walnuts, and often break down and suppurate.

Furunculosis, otitis media, pyelitis, and pneumonia are common. One striking feature is a blueness and coldness of the hands and feet; I think that this and the general glandular enlargement are the most important diagnostic signs. There is always a high white count even when there is no fever or other gross signs of infection. Most of the in­crease in white count is made up of eosinophils, which may reach 50 per cent of the total white cells. There is usually a strong seborrheic element, and the appearance of the skin may sometimes be almost exactly that of Leiner’s disease.

I look upon this syndrome as a combination of atopic and seborrheic dermatitis, and in the last few years have become convinced that over­growth of staphylococci or strepto­cocci on or in the skin and probable sensitization to them plays a dominant role in the clinical picture, and is the main reason why treatment is so un­satisfactory. The general glandular enlargement, the tendency of these glands to suppurate, the frequent occurrence of furunculosis, the high white count, and the frequent epi­sodes of fever, all point to infection.

Furthermore, it is not uncommon for the mother to develop small infected papules or pustules on her left fore­arm where the baby rubs his face when she is holding him, and she holds him a good part of the time because she has to rock him in order to keep him quiet. These babies not uncom­monly die. A few years ago I went over the autopsy protocols of twenty-six of them who had died in the In­fants’ Hospital. Nearly all died from infection, plus poor nutrition-septicemia, pneumonia, pyelitis, or otitis media. The most common organism recovered was the Staph. aureus.

There can be no doubt that emo­tional disturbances are of great im­portance in aggravating atopic derma­titis. That they are ever a primary cause, I do not believe, and I cannot agree with those who think that psy­chiatric treatment is the most im­portant thing in dealing with these patients. Like all good things, the psychiatric aspects of atopic dermatitis have been overemphasized. The older the patient, the more important psychiatry is; I am very doubtful that it has much to do with atopic dermatitis in babies, in spite of what some enthusiasts have said, except that when they are overtired or over­excited they scratch more. There can be no doubt, however, that in older children mental tension of any sort can aggravate the eczema. This is particularly true of girls and boys in high school or college who are con­scientious about their studies and are having difficulty with them-atopic dermatitis is always worse before an examination. I think a good deal of the necessary psychotherapy can be done by the pediatrician, but if it is obvious that there are deep-seated and long-standing psychiatric diffi­culties, he will do better to send the patient to a psychiatrist, for tech­niques which we do not have are necessary in dealing with such pa­tients.

It is not possible to avoid some environmental allergens, so that the question of hyposensitization naturally suggests itself. “Walker^“ in 1918 was the first to discuss this. He said: “Eczematous patients tolerate very small doses of the offending protein and the eczema seems to improve; but a slight increase makes the eczema worse. The amount of protein that benefits eczema is too small to prevent asthma, and the amount that benefits asthma makes the associated eczema worse. Desensitization for eczema must be a very slow and cautious process.” This was written thirty-seven years ago. It was true then; it is true now.

There is, however, considerable dif­ference of opinion as to the value of hyposensitization. Some place it on a par with hyposensitization in hay fever; some believe that it is worth­less. All are agreed with Walker’s original statement that very small doses of antigen must be used if exacerbations of the dermatitis are to be avoided. A severe exacerbation is no light matter, and it may be a good while before it calms down.

It has seemed to me that while hyposensitization is sometimes worth while, it can be by no means put upon the same plane as hyposensitiza­tion in hay fever. The situation is quite different. In hay fever the symptoms are brought about by local contact of pollen with the nasal mucosa; in atopic dermatitis due to pollen the pollen antigen has been ab­sorbed and brings about its effects from within.

If it is admitted that circulating pollen antigen causes the trouble, it is not logical to expect good results by adding more antigen to that which is already present. For this reason I am somewhat doubtful of the beneficial effects of such inocu­lations while the patient is still in his dusty house or during the pollen season. However, these are all ob­scure matters, with many questions un­answered, and I am sure that hypo­sensitization may sometimes do good. I have seen some patients made much worse by the injection of only a very small dose; I have seen some for whom attempted hyposensitization did no harm or no good; and I have seen a few where it was undoubtedly of real benefit.

For pollen dermatitis it is the only thing that can be done, except local treatment or treatment with cortisone. In the last two years I have given the inoculations intracutaneously rather than subcutaneously. Whether this is really any better than the subcutaneous method, I do not know. My recent practice has been to give once a week (later every two weeks) just enough extract (dust or pollen) to produce a reaction about as big as a nickel. In two pa­tients being treated now this is brought about by the injection of about 0.05 c.c. of a 1 to 10,000 pollen extract. The dose is not increased- no attempt is made to attain a maxi­mum tolerated dose as there is in treating hay fever; if you keep rais­ing the dose you will almost certainly reach the point where there will be an exacerbation of the eczema. I have taught one mother to give these intracutaneous injections-the dose is so small that there is no possibility of a general shock reaction.

Of the children with atopic derma­titis from wool whom I have seen, I have used hyposensitization in only three. These patients had such severe eczema that it was incapacitating. The dosage of wool extract used was 0.20 to 0.40 c.c. of a 1 to 10,000 dilu­tion given subcutaneously. One of these patients had a severe flare-up after a dose of 0.05 c.c. of a 1 to 1,000 dilution. It seemed to me, and to the patients, that hyposensitizing inocula­tions, which were done for several years in each case, were of definite benefit. The inoculations were started in September, carried through the winter, and discontinued in the sum­mer.

-Walker, I. C.: Causation of Eczema, Urticaria and Angioneurotic Oedema by Pro­teins Other Than Those Derived From Foods, J. A. M. A. 70: 897, 1918.

The environmental allergens which most frequently cause atopic derma­titis are house dust, pollen, and wool. In addition to these I have seen it caused by horse and cat dander, cot­tonseed, Kapok, and feathers. It is probable that these allergens, with the exception of wool, work by in­halation more than they do by con­tact.

For young infants, house dust and wool are the most important of the environmental allergens. Pollen as a cause of atopic dermatitis is unusual in infants-the youngest child that I have seen, in whom I was sure it was a cause, was 2 years old. If my figures for intracutaneous skin tests with dust and feathers mean anything, and I am not entirely sure that they do, these two allergens are frequent causes of atopic dermatitis in infants; this is, however, pretty hard to prove. As a routine treatment it is well to remove feathers from the environ­ment, and dust and wool in so far as it can be done. What one sees so often is a highly allergic baby with atopic dermatitis in whom it is diffi­cult to prove any specific clinical sensitivity except for egg white.

It is in children after the age of 2 years that the environmental allergens are most important, and if the eczema began late, that is, after the age of 10 or 12 months, and particularly if it began back of the knees and in front of the elbows instead of on the face, the chances are that it is due to environmental allergens. I am sure that many children after the age of 2 years have atopic dermatitis from house dust.

In children who have had atopic dermatitis for several years, a history of seasonal exacerbation is of the ut­most importance. Many of these chil­dren are worse in the winter and their eczema begins each fall, “as soon as the heat is turned on.” It lasts all winter, reaches its height in March or April, and then begins to subside, so that during the months of June, July, and August there is little or no eczema. Such eczema is often due to wool or to house dust or to both.

Another group of patients is nearly free from eczema in the winter, and has it especially during the pollen season, with or without hay fever. These patients are common, and it seems clear that their eczema is due to pollen. This is probably caused by inhalation of pollen, and not by contact (see Contact Dermatitis), for scratch tests of the urticarial type are positive, and patch tests with whole pollen or with pollen oil, at least in my experience, which is only with children, are negative. Still another group of children has atopic derma­titis all the year round. Sometimes these children are sensitive to dust and wool, which accounts for their winter trouble, and also to pollen, which accounts for their summer trouble, and some may be sensitized to still other environmental allergens such as feathers and animal dander.

I have seen a boy of 7 years, whose eczema was caused solely and entirely by feathers. He lived on a chicken farm where there were 2,000 chickens. Food is sometimes a partial cause of atopic dermatitis in older children but I think environmental allergens are of far more importance. This has been emphasized especially in the last few years by Louis Tuft of Philadel­phia, and he has quite definitely caused exacerbations of atopic derma­titis by spraying house dust into the nose of one patient and ragweed into the nose of another. I have seen much atopic dermatitis due to wool, although I am not quite so enthusias­tic about it as is Dr. Earl Osborne²¹ of Buffalo, who has studied this sub­ject for years. I think that wool works more often by contact than it does by inhalation. Dr. Osborne has pointed out, however, that what we call “house dust” is to a large extent made up of wool fiber, and he is con­vinced that it works as frequently by inhalation as it does by contact. How­ever, scratch tests to wool are uncom­mon, and when they do occur, the degree of sensitization is low. Wool is a weak allergen, although rarely the degree of sensitivity is so great that simple contact of wool with the skin will cause urticaria, and I have seen one child who wheezed if a wool blanket came near his nose.

²¹Osborne, Earl D., and Murray, Philip F.: Atopic Dermatitis. A Study of Its Natural Course, and of Wool as a Dominant Allerg-enic Factor, Arch. Dermat. & Syph. 68: 619, 1953.

Such situations are, however, unusual. In 200 cases I found only one positive scratch test. Dust, however, in older children with atopic dermatitis gives a high percentage of positive scratch tests (I have no accurate figures) and many of these are strong reactions. Furthermore, it has been clearly shown that while dust is made up of all sorts of small particles, and that a good many of these are wool par­ticles, the allergenic activity of dust depends not so much upon these as upon its own specific allergen.

Children with wool sensitivity are likely to have eczema around the neck, on the wrists and the back of the hands (mittens), and around the ankles, if they have been wearing a snowsuit, and the legs get wet, as they usually do. There is also likely to be eczema in front of the elbows and back of the knees which is prob­ably caused by absorption of the allergen from other localities or pos­sibly by inhalation. Wool is also irritating to many skins entirely apart from any question of allergic sensiti­zation.

In a recent series of forty cases of “winter” atopic dermatitis in children between the ages of 2 and 12 years I found no positive scratch tests to wool, ten positive intracutaneous tests, and fourteen positive patch tests. There was no correlation between the posi­tive patch and intracutaneous tests- either might occur without the other.

Fig.  24.-Atopic dermatitis from wool.    Easily treated because it can be bandaged.    Tar paste is indicated,   or  Swartz’s  ointment made without lanolin.

A positive patch test* is pretty good evidence that the eczema is being caused by wool, a positive intracutaneous test probably means very little one way or the other. A nega­tive patch test, on the other hand, by no means excludes wool as a cause of the eczema, because in the patch test the element of rubbing is not present, which is probably of consider­able importance in causing the eczema. It is not easy to avoid wool. What I have usually done is to have the children wear Byrd cloth or nylon snowsuits, leather mittens lined with cotton, cotton or nylon jerseys, re­move wool rugs from their bedrooms, and either get rid of their wool blankets or have them enfolded in cotton sheets.

“The wool patch should be left on for five days. The sensitivity is of low degree, and it is rare for a positive test to show if the patch is removed in twenty-four hours.

Orange Juice.-It is common for the mother to notice that the baby “breaks out” if orange juice is given. It is probably best to remove it from the diet of most infants who have atopic dermatitis, for orange juice is of little or no value to a baby except as an antiscorbutic, and if he is taking any “multivitamin” drops he is getting an adequate amount of vitamin C. If he is not, it is a simple matter to give him some ascorbic acid.

Positive scratch tests to orange are uncommon: in 300 cases there were only four. In a series of twenty-three tested by the intracutaneous method, however, there were eight slightly posi­tive tests. Sensitivity to orange is almost always of low degree-I have seen one 4-year-old child, however, who was exquisitely sensitive to it, and who had an enormous positive scratch test.

There are in orange juice three sub­stances which may produce allergic symptoms:

1. The  protein  of  the  juice
2. The protein of the seed
3. The peel oil

The relative importance of these is not entirely clear. In most commercially prepared orange juice there is plenty of chance for peel oil and seed protein to be present. Bib* canned orange juice contains no seed protein and no peel oil, and in five infants who had allergic symptoms from ordinary orange juice, Batner and his co-workers²⁰ found that the Bib juice was

tolerated. They do not say what sort of allergic symptoms were present. I have had no personal experience with it.

In orange juice, as it is prepared at home, it is not likely that any seed protein is present, and the amount of peel oil must be very small, although possibly enough to produce symptoms. The oil of orange peel in addition to being a sensitizer (its active principle is dextrolimonene, which is closely allied to turpentine) is a primary irri­tant, and dermatitis of the fingers from it has been known for a long time and is common in adults whose work in­volves the cutting up of oranges. It seems likely that if sensitivity to orange peel oil existed in infants it would be epidermal rather than dermal, and would therefore not be demonstrated by scratch or intracutaneous tests. Sensitivity to the juice protein or to the seed protein is shown by urticarial type scratch or intracutaneous tests. Ratner and his co-workers-” in a painstaking study showed clearly that the protein of orange juice is not readily absorbed from the digestive tract in an unsplit antigenic condi­tion, and said, “What we call allergy to citrus fruit may in truth not be al­lergy in all instances, but irritation from the peel.” This seems likely.

*Bib Corporation,  Lakeland,  Fla.

²⁰Ratner, Bret, Untracht, Samuel, Malone H. John, and Retsina, Mary: Allergenicity of Orange Studied in Man, J. pediat. 43: 421, 1953