Vitamin A For Keratosis Pilaris


Keratosis pilaris (KP) is a common skin condition that affects people of all ages, but it most often occurs in young children and teens. The condition causes small bumps to appear on the skin, especially on the backs of the arms and thighs.

KP can be treated with prescription-strength creams or lotions, but you can also try over-the-counter treatments that contain vitamin A. These treatments can help improve the appearance of KP by making it less visible and reducing the amount of redness that occurs when you apply your cream or lotion.

Vitamin A For Keratosis Pilaris

  • 23 Section of Dermatology 337
  • to reduce the exposure time to a minimum to prevent the definition from being impaired
  • by involuntary movement of the patient during the exposure, also to use a small concentrated light source to produce sharp shadows. Hence a powerful light source and
  • one of high actinic efficiency was required, and the Mazda 250 watt compact source
  • mercury vapour lamp was chosen. With this lamp, exposures of I4 second at f 16 using
  • panchromatic film (230 Scheiner) were adequate with the oblique lighting. The apparatus
  • was also designed to carry a photoflood lamp in a reflector to provide flat illumination,
  • as in some instances flat lighting was quite satisfactory.
  • With this apparatus the conditions of lighting on the skin are kept cQnstant as the
  • lamp is fixed in relation to the camera and to the skin. A rectangular aperture covering
  • the whole field of view of the camera is attached to it at such a distance that the
  • area enclosed by the aperture is in sharp focus. In using the apparatus it is arranged
  • so that the aperture surrounds and touches the area of skin being photographed.
  • Vitamin A and the Skin
  • By HUGH S. STANNUS, M.D., Ph.D., F.R.C.P.
  • As the result of observations made chiefly among native inhabitants of the Far East
  • a belief grew up that a specific type of dermatosis was due to a vitamin-A deficiency. The dermatosis was of the nature of a follicular hyperkeratosis, and was immediately adopted as a criterion of vitamin-A deficiency. The condition has, therefore assumed
  • some importance during the present war.
  • Whep in 1942 rapid nutritional surveys in Gyieat Britain, under, the aegis of the Ministry of Health, were initiated by Professor Sydenstrieker, “follicular keratosis” was one of t-he signs recorded as indicating a possible vitamin-A deficiency. v
  • These surveys were carried on by Dr. Brunel Hawes and myself and later continued by Drs. Adcock and Fitzgerald.
  • It soon became apparent that the follicular keratosis we were seeing in this country was very common, especially -among children, and further observations showed that it
  • was none other than keratosis pilaris.
  • Well known to dermatologists and recognized by them as a very common skin affection, it has been “rediscovered”, so to speak, by medical men who, interested in nutrition, but untrained in dermatology, may not recognize the condition. for what it is.
  • Already reports are reaching this country from until lately enemy-occupied countries concerning an affection which I believe to be identical with keratosis pilaris but which is not being recognized as such but rather considered as the follicular keratosis associated with possible vitamin-A deficiency, The most recent. reference is a letter in the Lancet of January (1945) mentioning the condition among East African native troops in Syria.
  • The condition as seen by us in this country has been recorded while passing in review between eight and nine thousand individuals, of whom more than half were children of school age attending pri,mary and secondary schools.
  • May I refer briefly to a few points: Among children of the 5-year-old gnoup the con- dition is seen in its minimal degree and simplest farm; as adolescence is 3pproached it becomes moxe,.marked and reaches its most exuberant form about puberty and during the next two. or three years, a time when the pilosebaceous glands reach their maximum activity and when hormonal influences may be playing a part; especially is this so among girls-and of these, among girls who are particularly well grown and plump.
  • There appears to be quite a definite seasonal incidence; the lesions become much more marked, fresh areas are involved or the eruption is remarked by the subject for the first time, with the onset of cold weather, and conversely with the coming in of warm weather. There appears to be some evidence too that lack *of protective covering-with exposure and trauma in its wide sense, such as friction and pressure-may also play a part. The follicular hyperkeratosis is not uncommonly associated with hyperkeratosis of the skin about the elbows and knees and in some cases, of the skin in front of the ankle-joints, to be distinguished from ichthyosis. Occasionally the follicles on the phalanges may be involved. Grubbiness with lack of *or but limited bathing facilities and absence of any kind of skin toilet may also be a contributory factor. In the more marked cases there appears to be a tendency to sonle increase of pigmentation of the skin in affected areas, mort especially around the lesions and also an associated acro- cyanosis.
  • The incidence of keratosis pilaris as noted by us has varied very much in different groups of individuals in areas’ In the 7-14 year tage-group among boys the incidence varied from 15 to 55%; among girls 15 to 80%; among male adults 0 to 5%; among female 3.5 to 20%.
  • Many of our percentages are higher than those given by Pemberton (1940). He found of 3,000 children examined that 5% exhibited “the fully developed condition”, and 20% simple enlargement of the hair-follicle, resembling permanent “cutis anserina”.
  • It may be of interest to re-examine the evidence which led’ to the belie! that certain changes in the skin, commonly referred to as “follicular keratosis”, were due to a vitamin-A deficiency.
  • 338 Proceedings of the Royal Society of Medicine 24The first description of the condition, one ascribed to vitamin-A deficiency, was given in an article by Frazier and Hu (1931) entitled “The cutaneous lesions associated with a deficiency in vitamin-A in man”, but these same lesions were noted many years before, in association with pellagra; by Majocchi (1902) who recognized what he referred to as seborrhceic, keratotic and acneiform follicular pellagroderms; and by myself in a group of African prisoners subsisting on a grossly deficient diet in 1911, i.e. before the vitamin era. It may also be noted that Seligman mentions seeing keratosis pilaris among the Papuo-Melanesian population of British New Guinea and Torres Straits during the ethnological expeditions of 1894 to 1904. The subjects referred to by Frazier were Chinese soldiers in Peiping whose diet was also a grossly deficient,.one but whereas in my own cases there were no jocular manifestations, in China the association with keratomalacia led Frazier and Eu to believe the condition was due to a vitamin-A deficiency.
  • The skin lesions preceded the appearance of the keratomalacia but (to,use their own words) “responded to therapy simultaneously with the ocular lesions but more slowly”. It should be noted, however, that therapy consisted in the administration of a well- balanced Chinese diet together with one lemon, liver, butter, eggs and 30 c.c. of cod-liver oil daily, so that in no sense was therapy of value as a differential diagnostic test.
  • The individual lesions and their distribution over the body differed in no way from those described by myself. They will be dealt with below. In 1936 Frazier and Hu published a second article covering a larger number of observations and said “further clinical observations tend to confirm the specific nature (i.e. due to a vitamin-A deficiency) of the hyperkeratosis of hair’ follicles”.
  • Meantime in 1933-that is two years after Frazier’s first article-Loewenthal (1933) published a paper upon “A cutaneous manifestation in the syndrome of vitamin-A deficiency”, occurring among prisoners in East Africa. This manifestation he believed to be “new”, as faras he was aware, but added that he had no access to the literature. His macro- and micro-scopic findings were similar to those noted by previous observers but of the latter he says: “These histological changes are precisely the same as those of the papule of pityriasis rubra pilaris though of course the two conditions cannot be confused clinically.”
  • Of 1,000 prisoners there were 81 with symptoms which might be referred to vitamin-A deficiency: 71 had night-blindness, 45 xerophthalmia and 75 exhibited the dermatosis. Treatment consisted in giving 1 ounce of cod-liver oil daily. Practically all were cured in rather over two months. To two cases 6 minims of avoleum were administered daily, i.e. a fish liver oil concentrate in cotton seed oil. “The xerophthalmia and night-blindness cleared up promptly, the dermatosis in eight weeks.”
  • Here again the diagnosis of the dermatosis as a vitamin-A deficiency depended upon the association with xerophthalmia and night-blindness and the response to substances containing the vitamin. No explanation is offered of the partial incidence of the affection among the 1,000 prisoners maintained on the same diet. In 1935 the same author reported finding a 30% incidence of this dermatosis among school children and 8 7% among adults of the general native population.
  • The same year (1933) Nicholls noted a similar condition of the skin among prisoners in Ceylon suffering from xerophthalmia and keratomalacia; and the following year reported it as common among native school children who at the same time exhibited signs of multiple deficiencies. The incidence among the children varied from 30% in a government school to 89% in a school for destitute children. The .average incidence
  • among over 4,000 children was 26-8%. In an asylum among males and females fed a Ceylonese diet the incidence was 44%; among the male inmates of another institution supplied with a European diet it was 2%. It must be noted, however, that none had ocular manifestations.
  • Nicholls invented the name “Phrynoderma”-toad skin-for the skin affection, rather unfortunately, I think, as it has served to perpetuate the idea of a specific entity due to a specific cause, viz. vitamin-A deficiency.
  • In 1936 Aykroyd and Rajagopal published their results of surveys among Indian school children. 16-5% of boys and 13% of girls in noorer schools exhibited “phryno- derma” and 6-6% of boys and 9.9% of girls in better schools.
  • These authors remark: “Phrynoderma is unquestionably due to dietary deficiency but evidence has been obtained that vitamin-A may not be the primary factor. . Phrynoderma may possibly be due to a deficiency of fat in the diet, to weather, to non-oiling.” There was a high incidence in cooler climates and during cold weather. They noted also that there was a lack of conformity between the incidence of phryno- derma and xerophthalmia and between phrynoderma and carotene intake in the diet.
  • In a paper the following year Aykroyd says: “Our observations are not incompatible with the theory that vitamin-A deficiency is one of the causative factors of phrynoderma, but the irregularity of its appearance in groups of malnourished children suggests some other factors may play a part.” The incidence of the condition among the children housed in 24 hostels each holding 65 boys or 74 girls were 0 to 53% of the boys, and 0 to 46% girls. In 1938 Rao remarked this skin condition among poorer class Indian children attending schools in the Nilgiris. The total number of children, the percentage affected and number treated are not mentioned.’ The treatment in two cases was as follows: To one boy aged 9, 10,000 i.u. vitamin A. as a concentrate. were administered daily with a good result in four months: the second case, a girl aved 6, responded to 18,000 i.u. daily in nine weeks. The photographs resemble perfectly those of keratosis pilaris, and it should be noted that untreated cases also improved.
  • The findings in a survey by Fasal (1944) may also here be mentioned. Among 1,482 Malays 2-0%’ and among 3.656 Indians 25-6% exhibited a’ follicular dermatosis which exactly resembled the condition found by others. The incidence among children was greater among females than males. Fasal believes the difference in diet is responsible for the racial difference in incidence. He found that red palm-oil with a vitamin-A
  • 25 Section of Dermatology 339
  • (? carotene) equivalent of 1,000 i.u. per c.c. by mouth or applied locally yielded excellent results, while coconut-oil, which contains no vitamin A or carotene, had no effect’ but that some cases did not improve unless the intake of protein was increased and vitamin-B complex added to the diet.
  • The correlation between the dermatosis and those symptoms which are more generally accepted as due to vitamin-A deficiency, is not always demonstrable. Pillat (1929), who
  • was particularly interested in the general signs associated with keratomalacia, described the skin as of a slaty grey or yellow colour, pasty and puffy in earlier cases, wrinkled and lined in later cases, with a dry feeling and a good deal of scurf due to hyperkera- tosis, with comedones on the face, but follicular lesions on the limbs and trunk were not mentioned.
  • The lack of a 100% incidence among individuals of a group under identical conditions has never been explained. Control observations have usually been wanting. The thera- peutic tests employed have generally not been exclusive. For many cod-liver oil has been synonymous with vitamin A. The preparations used may have contained other factors than vitamin A, and supplements to the diet have often been made at the same time, or improvement did not occur until supplemenfs to the diet were made.
  • The nearest approaches to an exact experiment are (1) the two prisoners given 6 minims of “avoleum”, a halibut oil concentrate, daily (by Loewenthal), whose dermatosis cleared up in eight weeks, and (2) a case reported by Frazier and Li (1938) which is stated to have responded in great part after fifty-one days’ treatment with 2 mg. carotene in olive oil given parenterally. How the carotene was prepared is not mentioned. Aykroyd, perhaps more than any other writer, appreciated some of the possible fallacies attached to the problem.
  • There is, however, one aspect of the subject which seems to have been overlooked by practically all observers, those mentioned already and others, namely, the possible relationship of the dermatosis under discussion with- any of the well-known skin con- ditions recognized by dermatologists. This may be accounted for I think, as I have already suggested, by two facts: very few of those engaged in work among native races in our colonies and elsewhere had had any dermatological training and, secondly, sur- rounded by a population living on what appear to be grossly unbalanced diets, the medical man had been inclined to see many illnesses through malnutritional spectacles. No one of the observers cited has ventured upon a differential diagnosis, and it is not without significance that Frazier, writing, from Texas in 1943, i.e. eleven years after his original paper, takes the trouble to state that “he never included in his published figures concerning follicular hyperkeratosis the common condition keratosis pilaris”, but he does not state how he made a differential diagnosis between the two conditions, which I believe to be identical. It might be stated here too that in this last paper Frazier, Hu and Chu report finding only 6-6% of follicular keratosis among 91 children with xerophthalmia of from 2 months to 15 years of age but 45-6% of 103 persons between 16 and 30 years exhibited the condition.
  • The character of the dermatosis supposedly due to vitamin-A deficiency as described by various observers is as follows: distributed symmetrically the eruption is generally profuse, although in some cases it remains localized. There is often some general dryness and roughness with scaliness and exaggeration of the skin creases giving rise to a wrinkled appearance, associated with hyperkeratosis. In other cases these changes are more or less localized to those areas presenting the typical follicular lesions.
  • These may appear rather suddenly in some one area and then extend rapidly until the characteristic distribution is attained, involving the anterolateral and posterior aspects of the thigh and the posterolateral surface of the forearm and arm with further extension to the leg and about the elbows, the buttocks, shoulders, axillary folds, the lower part of the abdomen and flanks, and finally the neck and face. The hands and feet are seldom mentioned but in some cases the follicles on the dorsal surface of the fingers may be affected.
  • At the same time some change in the colour of the skin may also be noted, varying according to race but most marked in the perifollicular region. Among the Chinese the colour is of a yellowish slaty tint, in dark-skinned races a deep brown or black, in white races a dusky purplish brown.
  • The characteristic lesion is a hyperkeratosis of the pilosebaceous follicles; they present as dry hard pigmented papules, 2 to 5 mm. in diameter, containing a central intra-follicular keratotic plug, many of which project from the hair follicles as horny spines or hard filamentous processes; or the follicle may be covered by a loosely adherent scale, in which case the lesion is conical or hemispherical in shape and may approximate in appearance, especially on the face, the comedo of acne, but pustulation does not occur. The plugs may fall out or be expressed leaving little gaping craters.
  • A broken hair may often be seen projecting from the centre of the follicle, or on extracting the plug, or removing the scale, a coiled-up hair may be found imprisoned within.
  • On section-there is found a progressive thickening of the epidermis with acanthosis as the follicle is approached. The follicle in its outer two-thirds is dilated and filled by a plug composed of concentric layers of keratinized material surrounding the broken or distorted hair. The proximal end of the follicle may be degenerated while the sebaceous glands are atrophied or indeed often completely destroyed. In the proximity of the follicle a mild cellular infiltration may be seen; all changes which are probably secondary to, the plugging of the follicle.
  • This clinico-pathological picture of so-called follicular keratosis or phrynoderma one believes to be identical with that met with in keratosis pilaris. While a follicular hyper- keratosis is a reaction common to a number of other skin affections, the condition above described may surely be differentiated from all of them.
  • 340 Proceedings of the Royal Society of Medicine 26
  • Clinically the condition described by Nicholls in Ceylon, so-called “phrynoderma”, by
  • Aykroyd in Southern India and by Fasal in Malay is very familiar to. Dr. Hawes as
  • seen among Malays, Indians and Southern Chinese and he identifies it with the condition
  • which he and I have been seeing in this country, while the condition as seen in Africa by
  • Loewenthal is also the same as recognized by myself.
  • Neither of us has seen the disease in Northern China where Frazier made his observations but we believe it to be identical on all the available evidence. Pemberton suggested that the condition in this country “is similar to those described by the older writers under
  • the names lichen pilaris, lichen spinulosus, nutmeg-grater skin and ‘scorbutic gooseflesh’ and is an early stage of the condition described by Pillat (1929), Frazier and Hu (1931),
  • Loewenthal (1933) and Nicholls as phrynoderma”, and he believed it to be an early sign
  • of a vitamin-A deficiency.
  • I would state, the case the other way round. The conditions observed among Chinese,
  • Indians,, Malays, Africans, &c., by these several authors is the same as that known to
  • dermatologists as keratosis pilaris, a condition which was at one time wrongly called
  • lichen pilaris and one which has nothing to do with scurvy. It is not a specific reaction
  • to vitamin-A deficiency. It should hlso be noted that Pillat did not mention the condition.
  • This is of course also true of a case under the care of Dr. Helen Mackay in London,
  • published by Goodwin (1934), which was supposed to have responded to vitamin A. All
  • the odd infective conditions, from diaper rashes upwards and downwards, which Dr.
  • Mackay (1934) supposed due to an A deficiency, similarly, I believe, had nothing to do
  • with such a deficiency.
  • In many of the groups of individuals examined by us in this country there could be
  • no question of an inadequate supply of vitamin A but in some areas this may not
  • have been true.
  • A more general lack of balance in the diet might well be a factor affecting adversely
  • those congenitally predisposed.
  • Any disturbance in a native’s normal diet is very likely to upset this balance. This
  • is well seen when he is confined in some institution, be it school, asylum or prison. It. is
  • well exemplified in imported Tamil labour in Malaya compared with the Malay
  • Dr. Hawes disagrees with me I think as to the paTt played by cold, exposure, &c.
  • It is difficult to disentangle possible factors in causation. Poverty, for instance, entails
  • at the same time poorer food as well as poorer and rougher clothing. The change into
  • the cold season may be accompanied by the disappearance of certain articles of diet.
  • Many native races are both poor, ill-fed, ill-clothed, unwashed and exposed. Even in
  • Singapore, with a temperature range of 90′ to 70°, a sudden drop to 70′ produces the
  • same effect as say a drop from 55′ to 40′ in this country.
  • This brings me to another point. Beres, in a Paris thesis (1928), refers to two adult
  • cases of keratosis pilaris, one under the care of Jeanselme, the other of Besnier, in
  • which the eruption appeared suddenly, in the one after a fall from a horse, in the second
  • case the exciting cause was exposure to cold, and suggests that the lesions remained
  • latent and unnoticed until excitation of the sympathetic caused them to become apparent.
  • This theory of sympathetic excitation acting upon- the erectores pilorum is not without interest in view of the effect of cold-and possibly of fear. As far as I know there is
  • no reference to these muscles in keratosis pilaris, but Nicolau (1918) described them as hypertrophied in the follicular lesions of scurvy met with in Serbian soldiers during the last war, an outbreak which was also the subject of an article by Wiltshire (1919).
  • The experimental production of skin changes comparable to those of supposed vitamin deficiency or of keratosis pilaris has been rather neglected. Moult’s work on the rat (1943) is, however, the most interesting. He submitted a series of groups of animals
  • to a series of diets, each containing less and less vitamin A, from 50 to 0 i.u. so that the progressive changes in the skin resulting from the degree of deficiency and the period
  • of deficiency could be studied histologically. The resulting pathological picture, including all the typical changes in the pilosebaceous follicle, closely resembles that seen in keratosis pilaris. The form in which the vitamin was administered is not mentioned but Dr. Moult has kindly informed me it was a fish liver oil concentrate of high potency diluted with edible ground-nut oil.
  • The matter is further complicated by the fact that for the absorption from the bowel
  • and storage in the liver of vitamin A other substances must be present, chief among these perhap! is tocopherol or vitamin E. These act as “anti-oxidants” or “protector” substances. It would be possible therefore to postulate a “conditioned” vitamin-A deficiency.
  • Again in turn the absorption and utilization of unsaturated fatty acids is bound up with an adequate supply of pyridoxin or vitamin B6, both concerned with the nutrition
  • of the skin.
  • (1) The condition called follicular keratosis, phrynoderma, &c., appears to be identical with keratosis pilaris.
  • (2) The actual pathogeny of the condition remains uncertain.
  • (3) It seems questionable whether a vitamin-A deficiency should be looked upon as a
  • specific cause, though under certain circumstances it may be a factor in causation.
  • (4) I would suggest that keratosis pilaris, as seen among all races, is a reaction in e
  • predisposed skin-to a disturbance in its normal metabolism. The disturbance may be in part traumatic, due to cold, &c., and/or in part nutritional, due to a relative lack of
  • some one or more essential food factors including vitamin A, vitamin E, vitamin B and fatty acids, associated with dietetic deficiency or deficient absorption.
  • 27 Section of Dermatology 341

keratosis pilaris causes

Keratosis pilaris (ker-uh-TOE-sis pih-LAIR-is) is a common, harmless skin condition that causes dry, rough patches and tiny bumps, often on the upper arms, thighs, cheeks or buttocks. The bumps usually don’t hurt or itch.

Keratosis pilaris is often considered a variant of normal skin. It can’t be cured or prevented. But you can treat it with moisturizers and prescription creams to help improve the appearance of the skin. The condition usually disappears by age 30.

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Keratosis pilaris can occur at any age, but it’s more common in young children. Signs and symptoms include:

  • Painless tiny bumps, typically on the upper arms, thighs, cheeks or buttocks
  • Dry, rough skin in the areas with bumps
  • Worsening when seasonal changes cause low humidity and dry skin
  • Sandpaper-like bumps resembling goose flesh

When to see a doctor

Treatment for keratosis pilaris usually isn’t necessary. But if you’re concerned about your or your child’s skin, consult your family doctor or a specialist in skin conditions (dermatologist).

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Keratosis pilaris is caused by the buildup of keratin — a hard protein that protects skin from harmful substances and infection. The keratin blocks the opening of hair follicles, causing patches of rough, bumpy skin.

It’s not clear why keratin builds up in people with keratosis pilaris. It may occur in association with a genetic disease or with skin conditions such as atopic dermatitis. Dry skin tends to make keratosis pilaris worse.

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