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  In this article
    Abstract
    Definition
    Aetiology and pa...
    Water content
    Water binding ca...
    Barrier function
    Environmental fa...
    Surface area
    Desquamation of ...
    Sweat and sebace...
    The causes of dr...
    Clinical manifes...
    Treatment
    References

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CONTINUING MEDICAL EDUCATION
Year : 2003  |  Volume : 69  |  Issue : 2  |  Page : 69-75

Dry skin conditions, eczema and emollients in their management


Dept. of Skin & STD, JJM Medical College, Davangere - 577 004, Karnataka

Correspondence Address:
"Prakruthi", 2830, 4th Main, MC Colony, 'B' Block, Davangere - 577 004, Karnataka

   Abstract 

Dry skin, which refers to roughened, flaky, or scaly skin that is less flexible than normal and dry to feel, is relatively common problem in all age groups, but is more common in elderly individuals. The water content of the stratum corneum is of paramount importance in maintaining the normal appearance and texture of human skin. The relative hydration of the stratum corneum is a composite of 3 factors viz. the rate of water transport from dermis to stratum corneum, the rate of surface loss of water and the rate of water binding ability of stratum corneum. Loss of integrity of the barrier function is a central factor in the development of dry skin conditions and eczema. The various factors involved in producing dry skin, various causes of dry skin and the role of emollients in the management of these conditions are discussed.

How to cite this article:
Siddappa K. Dry skin conditions, eczema and emollients in their management. Indian J Dermatol Venereol Leprol 2003;69:69-75


How to cite this URL:
Siddappa K. Dry skin conditions, eczema and emollients in their management. Indian J Dermatol Venereol Leprol [serial online] 2003 [cited 2014 Jul 26];69:69-75. Available from: http://www.ijdvl.com/text.asp?2003/69/2/69/5876


Dry skin is not a unique, well defined condition, but represents a medley of total; unrelated changes in the structure of the stratum corneum which is associated with decreased water content of the stratum corneum. Many causes car induce dry skin through a number of biologic pathways.[1] Dry skin is a relatively common problem in all age groups but is more common it elderly individuals.
Synonyms are xerosis, xeroderma aesteatosis, winter itch, dermatitis hiemalis, etc The self descriptive term, dry skin is morE preferable than the others.

   Definition Top

Dry skin refers to roughened, flaky o scaly skin that is less flexible than normal and dry to the touch. Follicular accentuation is offer prominent on extensor surfaces and the condition is aggravated by cold, dry climates or Seasons.[2]

   Aetiology and pathogenesis Top

The surface of the human skin normally feels smooth and supple as opposed to the harsh and brittle scaly surface of dry skin and there is no visible scale on the surface.[1] Many factors are responsible for maintaining the normal appearance of the skin.

   Water content Top

The water content of the stratum corneum is of paramount importance in maintaining the normal appearance and texture of human skin and the relationship between water and dry skin is Complex.[3] The relative hydration of the stratum corneum is a composite of 3 factors viz. the rate of water transport from dermis to stratum corneum, the rate of surface loss of water and the water binding ability of stratum corneum.[4] Stratum corneum is soft and pliable when its water content reaches 10mg/100mg dry weight, corresponding to 60 percent relative humidity.[3] As relative humidity increases, transepidermal water loss falls.[5] Surface ventilation also accelerates water evaporation. Cold, dry and windy climates enhance water evaporation. Skin dryness has also been shown to worsen with increasing dew point.[2]

   Water binding capacity Top

Available evidence indicates that the water content of the normal stratum corneum is largely dependent upon the intracellular water soluble hygroscopic substances (Natural Moisturing Factor), enveloped in lipid membranes.[6] These substances can be extracted with water only after treating the stratum corneum with various lipid solvents or detergents.[2] Individuals exposed to lipid solvents or detergents may therefore, have a propensity to loose naturally occurring hygroscopic compounds and develop dryness and scaling of the skin. Natural Moisturing Factor (NMF), comprising 30 percent of stratum corneum, is actually a collection of several compounds including 40 percent free aminoacids, 12 percent prolidine carboxylic acid, 12 percent lactate, 7 percent urea, minerals, electrolytes and sugars.[4]
If the stratum corneum has decreased water binding capacity, it will contain less water than normal under any set of atmospheric conditions and might lead to dryness.[6] In ichthyosis, stratum corneum has a dimished water binding capacity in vitro compared to stratum corneum from control subjects. Any physiological condition which decreases the water content of the stratum corneum may lead to tautness and scale formation. Conversely hydration of the stratum corneum makes it more pliable.

   Barrier function Top

Skin acts as a two-way barrier to prevent the inward or outward passage of water and electrolytes.[7] This barrier function is largely localized to the stratum compactum of the horny layer,[6] and depends on both cornified material of the keratinocytes and the intercellular lipids[7] that have been released from the lamellar bodies (Odland bodies, membrane coating granules) in the underlying stratum granulosum.[8],[9] The intercellular lipids undergo enzymatic processing to produce a lipid mixture of ceramides, fatty acids and cholesterol.[10] These molecules are arranged in a highly organized multilamellar fashion fusing with each other and the corneocytes to form the skin's lipid barrier.[9] In addition the water soluble hygroscopic substances within the keratinocytes allow them to retain moisture and cause them to swell and press into one another, preventing cracks and fissures.[11] The currently accepted view is that the proteinaceous keratinocytes are embedded within a continuous lipid-rich matrix and act as a barrier.[7] The fibrous proteins of keratin and a histidin-rich protein known as keratohyalin or filaggrin are synthesized within the keratinocytes.[12] An envelope, formed by cross-linking of the precursors-volucrin and keratohyalin around each keratinocyte, forms an exoskeleton and acts as a rigid scaffold for the internal keratin filaments.[13] There is evidence that lipids are chemically bound to the surface of the corneocytes.[14]
Important intercellular stratum corneum lipids implicated in the barrier function are ceramides, free fatty acids and free sterols.[15] Transepidermal water loss is necessary to stimulate the lipid synthesis. The major lipid by weight found in the stratum corneum is ceramide (sphingolipid). Ceramides possess the majority of the long-chain fatty acids and linoleic acid in the skin.[16] Other lipids present in the stratum corneum are triglycerides, squaline, sterol wax/esters, n-alkanes and cholesterol sulphate. Cholesterol sulphate which comprises only 2-3% of the total lipids is important in corneocyte desquamation. It appears that corneocyte desquamotion is mediated through the desulfation of cholesterol sulphate.[17]

   Environmental factors Top

Temperature and climate are important determining factors of the state of the normal skin which have their effects on the abnormally dry skin and in the hydration. There is a gradient between the water content of the stratum corneum and the atmosphere. Low relative humidity and high wind velocity tend to remove water from the stratum corneum and cause chafing or mild scaling even in most normal individuals. Dryness and scaling of the skin tend to improve spontaneously during the summer months due to heat and humidity and become more severe during the winter months.[18]

   Surface area Top

Ordinarily the surface areas of the stratum corneum and subjacent epidermis and lower skin layers should be precisely equal. When the stratum corneum is drier than normal, its volume and surface area shrink. Dry stratum corneum has less surface area than tissues below and the skin surface first becomes taut and then cracks to form scales or fissures where the stratum corneum is very thick, as in soles. Scale formation is associated with defective barrier function.[18]

   Desquamation of cells Top

At any point the number of cells arriving at the surface and those being shed is approximately equal except during the period when scales are accumulating, then the rate of cell production exceeds the rate of cell exfoliation. Horny cells of the stratum corneum are cemented together to form a membrane and are continuously shed from the surface, desqumating at fixed level in relatively large clusters at the point where the binding forces between horny cells can no longer withstand external abrasive forces. The binding (or cohesive) forces within the stratum corneum decrease during the ascent of horn cells from the granular layer to the surface. When the intracorneal cohesion is abnormally high, cells remain attached instead of separating and scaling or hyperkeratosis occurs. Hyperproliferative or retention hyperkeratosis occur depending upon whether there is increased or normal proliferation of epidermal cells.[19]

   Sweat and sebaceous glands Top

Sweat glands and sebaceous glands help in maintaining the smoothness and suppleness of the skin by providing water and the fatty film on the surface of the skin respectively.

   The causes of dry skin Top

The causes of dry skin are centered around three overlapping areas: lack of water in the stratum corneum, overactive epidermal turnover, and barrier damage.
If the stratum corneum is desiccated, the result is dry skin.
Chornic low level irritation either from chemicals, UV exposure, or in most dermatitides, can increase turnover of cells as part of the inflammatory process. When this occurs, there is inadequate time for the keratinocytes to differentiate properly and the appropriate lipids to be produced. The result is a defective barrier that cannot hold water and the result is dry skin.
The third major cause of dry skin is barrier damage. When there is depletion of the intercellular lipids, such as with detergent exposure during dish washing, the barrier is damaged and the rate at which water traverses the skin from within is markedly increased. If the water cannot be stopped at the stratum corneum level, then desiccation of the outer surface of the skin occurs and produces dry skin.[20]
There are multiple causes of dry skin. It may be acquired, constitutional and genetic in origin. It may be localized dry skin in each of the conditions of genetic origin is probably related to a single biochemical defect in the corneocytes. In that group keratins, filaggrin, keratolinin, involucrin, cholesterol sulphatase, membrane coating granules and so many other molecules and organelles play critical roles.[1] Ichthyosis, the dry skin of anhydrotic type of congential ectodermal defect, and dry skin of atopic dermatitis-as a result of abnormal barrier function due to ceramide distribution[21] (also observed in psoriasis)[22] a genetic defect in the metabolism of essential fatty acids (lack of 6-6 desaturase)[23] are examples of irreversible types of dryness of skin of genetic origin. Ichthyosis constitutes a heterogenous group of genetic and acquired disorders characterized by a generalized persistent non-inflammatory scaling of the skin surface. They are generally disorders of keratinization.[24]
Acquired dry skin may arise from normal (or sometimes even from greasy) skin, which is rendered temporarily and locally dry by external factors including solar (UV) radiation; exposures to extremes of climate: cold, heat, wind, dryness; exposure to chemicals: detergents; and various therapeutic measures(e.g., retinoids).[23]
Generalized acquired dryness of the skin is symptomatic of the acquired, chronic, wasting, systemic diseases as well as of the generalized cutaneous atrophy in the aged. Interestingly enough xerosis tends to increase with age due to a lower inherent water content of the stratum corneum[25] and also probably due to an abnormal desquamatory process.[26] Dryness may be due to decreased activity or atrophy of the sweat and/or sebaceous glands (endocrine disturbances, drug effects, cutaneous malnutrition) or to dehydration of the skin caused by errors in water and protein metabolism (toxaemias and wasting disease).
Dryness of the skin may also develop in constitutionally predisposed individuals as a result of exposure to low ambient relative humidity and low temperatures, made worse by frequent bathing and vigorous toweling after wards.[23]
Minor dry skin (xerosis vulgaris), probably of genetic origin, is found frequently in women, usually those with a pale phototype. Xerosis affects particularly the face, back of hands and limbs.[23]
Loss of integrity of the lipid barrier is a central factor in the development of dry skin conditions and eczema. The apparent sharp rise in the prevalence of eczema in the recent years suggests that environmental factors contribute to promoting barrier dysfunction. Factors such as frequent washing with soap products, exposure to irritants, bacteria or house dust mite and dry environments may all contribute to loss of barrier function as well as leading to exacerbation of existing dry skin conditions and eczematous conditions.[27] Washing with conventional soap products can have a drying effect on the skin, removing lipids and reducing the thickness of the stratum corneum.[28] Many soaps and cleansing products contain sodium lauryl sulphate, a detergent with known irritant properties.[29] Low humidity, such as that created by air-conditioning, induces profound changes in epidermal proliferation and function.[30] Injury to the stratum corneum from these or other causes provides increased opportunity for irritants and allergens to penetrate the skin and promotes the release of inflammatory cytokines.[31] These effects, which are subtle initially, may lead to the development of dermatitis, when they accumulate progressively until threshold is reached. Sensitivity thresholds towards irritants and allergens vary considerably among individuals and may be influenced by genetic as well as environmental factors.
Dry skin and poor complexion complained by many young and middle aged women appear to be due to excessive use of soaps, cosmetics, dyes, perfumes, etc. containing irritating or allergenic ingredients. Similarly the dryness of the skin and itching is complained by many middle aged patients, particularly women. Often such itching is aggravated on dressing or undressing, after bath or at night, and it appears to be due to a combination of factors including hot baths (too long, too frequent and too hot) and the excessive use of soaps, perfumes, bath salts, etc. The cure for this type of dryness of skin lies in limiting or avoiding such excesses and if necessary, addition of emollient preparations to the bath.
Excessive dryness is also a common complaint in persons who come in contact with highly alkaline soaps and detergents (housewives, dishwashers, launderers, surgeons, etc.), organic solvents or alkalis, irritating dusts and cleaners (mechanics, cement workers, etc.) Reduction of exposure to the irritants, the use of protective gloves and the application of emollient ointments and crams are indispensable to the treatment. Cleansing measures should be limited to the use of mild toilet soaps, super fatted soaps, oils and creams.

   Clinical manifestations Top

The earliest change noticed in the skin is fine accentuation of skin markings, followed by irregular or reticulate superficial red fissuring. As the dryness increases, roughness and scaling develops. Increased scaling may instead suggest ichthyosis vulgaris. These changes are often most pronounced over the anterior and sides of legs, extensor aspect of arms and forearms, and dorsa of hands. Body folds are usually spared. Pruritus which may be localized or generalized, may lead to development of dermatitic changes.[32]
The degree of dryness and scaling varies with the specific disturbance as well as its severity. In the anhydrotic type of congenital ectodermal defect the skin is dry, but rarely excessively scaly. In cachectic states scaling is superficial, finer, branny or lamellar. In ichthyosis the skin is excessively dry and scaly.
There appears to be an inherited susceptibility, a positive family history and this is especially true in patients with an atopic diathesis. Dry skin is common in elderly but is frequently found in patients with atopic dermatitis, hypothyroidism, uraermia and lymphoma. Important contributing environmental factors include low humidity, sudden skin cooling by air conditioning, dry heat, cold weather, and wind.[2]

   Treatment Top

The relief and prevention of dryness of the skin is centered around the maintenance of proper hydration of the stratum corneum. Restoration of barrier function is of paramount importance in controlling dry skin conditions and eczema.[27]
Elimination of irritants and soap products is regarding as an important first step. The detrimental effects of soap are widely recognized by the sufferers of eczema. In a recent survey in U.K. 38% of respondents showed a flare-up of their eczema after washing with soap. In such instances a soap substitute bar, cream or lotion should be used as an alternative cleansing agent.[27] In case of cleansing creams, they are spread on the skin surface with the fingers and then wiped with a tissue or water-rinsed if they are water­rinsable cold creams, made of natural waxes and mineral oils with borax as an emulsifier.[32]
Emollients and moisturizers are often referred to synonymously and perform similar functions in adding moisture to the skin. They are the first-line treatment for dry skin conditions and eczema. Traditionally, emollients provide an inert oily layer over the surface of the skin. Emolliments, which can be in the form of ointments, creams, lotions, or bath oils, are commonly recommended as a means to improve barrier function and to relieve feelings of dryness and pruritus.[27]
Emulsions are the most common form of moisturizers. The rate of water loss from the horny layer may be impeded by using emulsions of oil­-in-water. The residual film of oil on the skin surface prevents or at least impedes evaporation of water from the surface of the skin and slows down the rate at which water is traversing the skin, thus trapping it in the upper layers of stratum corneum, allowing for softening and smoothening the skin surface. It is this form of cream that is being used by the persons with very dry skin and the persons who are frequently exposed to winter weather.[20]
Binding of water at the skin surface is accomplished by humactants that are capable of retaining large amounts of water relative to their weights. The traditional humactants such as glycerine and glycols are now replaced by biocompatible agents such as hyaluronic acid and mucopolysoccha rides.[20]
Delivering and binding water at the skin surface does not solve the problem of dry skin, but by increasing internal water binding capacity the dry skin problem is more dramatically improved. Modern moisturizers containing derivatives of vitamin A such as retinlyl palmitate, by stimulating the synthesis of glycosaminoglycans can increase water retention in both the epidermis and dermis. Glycosaminoglycans, long chain amino-sugars, bind water at concentrations many times their weight, resulting in increased internal water retension within the skin. This internal moisturization compliments the delivery of water externally to the skin surface. The aspect of dry skin condition, which is due to increased turnover rate of epidermal cells caused by chronic irritation, can be effectively handled by incorporating agents such as combination of vitamin of vitamin-A palmitate and 7-dehydrocholesterol, that help to regulate the differentiation process so that equilibrium can be reestablished.[20]
Emollients are often used incorrectly. They are most effective when applied after bathing, when the skin is still wet, and ideally should be re-applied regularly throughout the day for maximum benefit. Correct use of emollients also has steroid sparing effect. However, it is important to note that the use of emollients alone is unlikely to control inflammation and topical corticosteroids should be used for a short period to control inflammation with continued use of emollient therapy, even when the visible sings of inflammation are gone (complete emollient therapy).[27],[33]
The choice of emollient depends upon the area of the body and the degree of dry ness of the skin. Lotions are used on scalp and other hairy areas, creams on face, trunk and limbs and ointments for drier, thicker and more scaly areas. Bath oil deposits a thin layer of oil on the skin upon rising from the water.[34]
A simple set of practical guidelines proposed for the use of emollients in order to facilitate effectiveness and consistency of emollient care are: (1) The health care professionals involved in the care of the patients with dry skin conditions and eczema should have knowledge of the basic principles of emollient use. (2) Patients should avoid soap and use an alternative cleansing agent such as a soap substitute bar or cream for washing, bathing and showering. (3) Even when the skin condition is under control, a daily emollient routine should be an important part of the management (4) The relative benefits of the steroid creams (to reduce inflammation) and emollients (to combat dry skin) should be understood by the patients. Any treatment regimen following these guidelines can then be tailored according to the patients individual needs and preferences.[27]
The patients should also be advised to avoid exposure to precipitating factors that aggravate dryness of the skin and to reduce frequency of bathing, have brief baths or showers, and use lukewarm water instead of very hot water for bath and apply an emollient liberally after bathing when the skin is still wet.[34]
In the congenital anomalies, no casual treatment is possible, but to some degree, these patients can be helped by residence in a warm, humid climate, wearing correct clothing (soft, non­-wooly materials), avoidance of soap, gentle massage with softening creams, emulsions or oily preparations and the administration of vitamin A. When the patient cannot move to a more suitable climate, the alternative palliative treatment is the daily application of hypertonic sodium chloride in cream form or hypertonic 3 percent saline baths. This simple inexpensive treatment often brings about remarkably rapid and far-reaching reduction of scaling and considerable relief from discomfort in many cases of ichthyosis and other forms of congenital or acquired dry scaling may be obtained as long as the therapy is continued.
In acquired forms of dry skin, systemic treatment consists chiefly of treatment of the underlying cause. In patients whose general health is not impaired, daily sweat baths (in steam rooms, when possible) and gentle massage with cold cream, mineral oil or a soothing emulsion are beneficial, and antipruritics may be added if needed. The addition of emollient preparations such as starch (I b) or Bran (1/4 lb), oatmeall extract 1 to 2 cupfulls to the tub bath is temporarily soothing. Excessive dryness of skin of bedridden patients is sometimes caused or aggravated by the bed linens. Bed clothes should be repeatedly rinsed in plain water to remove all traces of soaps, bleaches, etc.
Innumerable proprietary and cosmetic preparations are available for the treatment of dry skin. The effects of most of them depend on their content of cholesterols, vegetable oils, cetyl alcohol, mineral oil, petrolatum, lanolin, etc. 

   References Top

1.Pierars GF What does "dry skin" mean?. Int J Dermatol 1987; 26: 167-168.  Back to cited text no. 1    
2.Demis DJ. Unit 1-19: Dry skin. In: Clinical Dermatology Twelfth Revision. Edited by Demis, Crounse, Dobson, Mcguine. Harper & Row; Philadelphia, 1985; P1-2.  Back to cited text no. 2    
3.Blank IH. Factors which influence the water content of the stratum corneum. J Invest Dermatol 1952; 18: 433-440.  Back to cited text no. 3    
4.   Back to cited text no. 4    
5.Fisher AA Irritant reactions from topical urea preparations used for dry skin: Advantages of a urea-free "Dead Sea Salt" cream. Cutis 1976;18:761-772.  Back to cited text no. 5    
6.Bettley FR, Grice KA. Influence of ambient humidity on transepidermal water loss. Br J Dermatol 1967; 79: 575-581.  Back to cited text no. 6    
7.Blank IH. Further observations on factors which influence the water content of stratum corneum. J Invest Dermatol 1953; 21: 259-269.  Back to cited text no. 7    
8.Archer CB. Functions of the skin. In: Rook/Wilkinson/Editing Textbook of Dermatology, 6'h Edn. Edited by Champion RH, Burton JL, Burns DA, Breathnach SM. Blackwell Science: London, 1998; P 113-122.  Back to cited text no. 8    
9.Odland GF, Holbrook KA. The lamellar granules of epidermis. In: Mali JWH ed. Current Problems in Dermatology. Basel:Karger, 1981: P29-49.  Back to cited text no. 9    
10.Wartz PW. Lipids and barrier function of the skin. Acta Derm Venereal 2000; 208 Suppl: P7-11.  Back to cited text no. 10    
11.Eleas PM, Wood LC, Feingold KR. Epidermal pathogenesis of inflammatory dermatosis. Am J Contact Dermat, 1999; 10(3): 119126.  Back to cited text no. 11    
12.Cork MJ. The importance of skin barrier function. J Dermatol Treat 1997; 8: PS7-13.  Back to cited text no. 12    
13.Baden HP, Lee I.D. Fibrous proteins of human epidermis. J Invest Dermatol 1978; 71:148-151.  Back to cited text no. 13    
14.Goldsmith LA. The epidermal cell periphery. In: Biochemistry and physiology of the skin, edited by Goldsmith LA, Oxford University press: New York, 1983: P184-196.  Back to cited text no. 14    
15.Swartzendruber DC, Wertz PW, Madison KC, et al. Evidence that the corneocyte has a chemically bound lipid envelope. J Invest Dermatol 1987; 88: 709-713.  Back to cited text no. 15    
16.Elies PM. Lipids and the epidermal permeability barrier. Arch Dermatol Res 1981; 95: 270.  Back to cited text no. 16    
17.Petersen RD. ceramides key components for skin protection. Cosmel Toilet 1992; 107: 45.  Back to cited text no. 17    
18.Long SA, Wertz PW, Strauss JS, et al. Human stratum corneum polar lipids and desquamation. Arch Dermatol Res 1985; 277: 284.  Back to cited text no. 18    
19.The epidermis. In: Dermatology, edited by Pillsbury DM, Shelly WB, Kligman AM. Saunders: Philadelphia, 1957: P7-14.  Back to cited text no. 19    
20.Klingman Am. The Horny layer In: The Epidermis. Edited by Montagna W, Lobitz W.C, JR. Academic press: New York, 1964: P287.  Back to cited text no. 20    
21.Maes DH, Marenus KD. Cosmatology for Normal skin. Main finished products: moisturizing and cleansing creams. In: Cosmetic  Back to cited text no. 21    
22.Deramotology. Edited by Baran R, Maibach HI. Martin Dunitz: London, 1995:77-87.  Back to cited text no. 22    
23.Imokawa G, Abe A, Jin K, et al. Decreased levels of ceramides in stratum corneum of atopic dermatitis: an etiologic factor in atopic dry skin. J Invest Dermatol 1991; 96: 523.  Back to cited text no. 23    
24.Motto S, Monti M, Sesana S, et al. Abnormality of water barrier function in psoriasis. Arch Dernotol 1994; 130: 452.  Back to cited text no. 24    
25.Gaily Y, Chappuis JR Skin care priducts for normal, dry and greasy skin. In: cosmetic Dermatology. Edited by Baran R, Maibach HI. Martin Dunitz: London, 1995: P89-1 10.  Back to cited text no. 25    
26.Nicholls s, et al. Ichthyosis. In: Ichthyoses. Edited by Marks R, Dykes PJ. MTP press: Lancaster, 1 978:P95.  Back to cited text no. 26    
27.Potts RO, Buras EM, Chrishman DA. Changes with age in the moisture content of human skin. J Invest Dermatol 1984; 82: 97.  Back to cited text no. 27    
28.Wepierre J, Marty JR Percutaneous absorption and lipids in elderly skin. J Appl Cosmetol 1988; 6: 79.  Back to cited text no. 28    
29.Holden C, English J, Hoare C, et al. Advised best practice for the use of emollients in eczema and other dry skin conditions. J Dermatol Treat 2002; 13: 103-106.  Back to cited text no. 29    
30.Cork MJ. The importantce of. skin barrier function. J Dermatol Treat 1997; 8: PS7-13.  Back to cited text no. 30    
31.Tupker RA, Willis C, Berardesca E, et al. Guidelines on sodium Layryl sulphate (SLS) exposure tests. A report from the standardization group of the European society of contact dermatitis. Contact Dermatitis 1997; 37: 53-69.  Back to cited text no. 31    
32.Denda M. Influence of dry environment on epidermal function. J Dermatol Sci 2000; 24 (suppl 1): PS22-28.  Back to cited text no. 32    
33.Elias PM, Wood LC, Feingold KR. Epidermal pathogenesis of inflammatory dermatosis. Am J Contact Dermat 1999; 10: 119-126.  Back to cited text no. 33    
34.Chernosky ME. Dry skin and its consequences. J Am Med Won, Assoc 1972; 27: 133-145.  Back to cited text no. 34    
35.Martin EW, Cook EF eds, Remingtor s Practice of Pharmacy, Back to cited text no. 35    
36.Cork MJ. Complete emollient therapy. The National Association of Fund Holding YearBook. Scorpio: London, 1998.  Back to cited text no. 36    
37.Mahajan DM. Caring for the dry skin. Dermagrace 2003; 2: 2 & 5.  Back to cited text no. 37    

 

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