Yes I am talking about the Nueslim diet pills. These are the ideal diet pills with all the natural ingredients, therefore do not require prescription. You can even purchase them online without any hassles whatsoever. Go online, order your requirement, pay by whatever means suitable to you, and get your pack of diet pills at your doorstep! Purchasing diet pills were never so easy.

Why these diet pills do not require any prescription is in almost all cases, not a single case complains of any complications or side effects after taking the pills. Rather they feel an energizing effect along with significantly losing weight. You will find yourself losing weight right in the first week of starting the treatment. If you are unhappy, return the package and get back your money. Yeah, the diet pills come with a lifetime money back guarantee too. So much the manufacturers believe in their product and now you will believe too after you start using it regularly!

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Most people desire an ultimate solution that will put them on right track and will ensure quality physical fitness along with shiny hair and skin. If a single pill is capable of doing all these things for you, why not opt for it? Yes, I am talking about NV. It is an “all-natural” diet supplement that offers effective weight loss. NV does it because of metabolic fat burners like green tea. Because of presence of Hoodia gordonii in NV, it acts as a good appetite suppressant and renders a false fullness.

NV also provides you anti-aging collagens and collagens for smooth skin. When you get all these ingredients in one single product, why to opt for anything else? Just start on NV right away and find yourself blooming with svelte figure and sexy outlook on life. Basically getting slimmer is getting committed to your bodily needs. Start with well-planned exercise regime and diet specifications along with NV. It is not a far dream then to realize your potential!

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The volcano vaporizer available in the market will suit your needs of achieving better health benefits. The people can make use of these vaporizers which can be safely used as an alternative to smoking also. Yes, smoking is injurious to health and passive smoking is more injurious to health. So, if you cannot curb your habit, at least do not let those around you to succumb to the bad effects of passive smoking. This is hundred percent achieved by vaporizers.

You smoke through the vaporizers and you spare yourself too of the bad effects of harmful gases like carbon monoxide and dioxide released during burning of plant material. This is because the vaporizer does not yield these gases as it heats the plant material at an optimal temperature lower than that of burning and does not yield tar. So, those around you will definitely thank you for your cooperation by using volcano vaporizer!

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It is also said that what you wear depicts your personality. So, if you wear pearl jewelry it says volumes about your style and psyche. Your companions will surely be envious about your pearls that are so good to say the least. The pearls are an apt expression of your personality. Why not take advantage of online sales that are soaring sky heights? People are crazy behind the latest patterns and designs in pearl jewelry.

You need not feel that your pearl jewelry cannot have varieties. Just hit an online pearl gallery and you will understand how many different types pearls can have! There are fresh water pearls, Tahitian pearls, black pearls, south sea pearls, Akoya pearls and numerous varieties of these pearls that are on display online. Womenfolk are literally head over heels in love with these pearl necklaces, bracelets and earrings. Even men are dying for pearl cufflinks, bracelets etc. if pearls are in so much demand these days, It would be a shame not to have ones for your jewelry collection!

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1. Distribution - trunk, buttocks, and thighs
2. Stability of plaque shape and size

Parapsoriasis is not, of itself, a very important disease. It is uncommonly encountered, is not contagious, and probably is not be cured, Its importance lies in its relationship to the cutaneous T-cell lymphoma (CTCL) mycosis fungoides. These two diseases exist on a spectrum such that over a number of years the lesions of parapsoriasis tend to evolve into those of the always fatal, mycosis fungoides.

Clinical Presentations

Several vanetles of parapsoriasis exist, but only the most common one, large plaque parapsoriasis (parapsoriasis enplaque), is discussed here. The lesions of parapsoriasis consist of sharply marginated, scaling, barely elevated, red plaques.as the name suggests, the appearance of these plaques is somewhat similar to those of psoriasis. In parapsoriasis, however, the color is brown red rather than bright red, the scale is line and powdery (pityriasis type) rather than flaky; and evidence of the Koebner phenomenon is not found. Finally, the plaques of parapsoriasis are extraordinarily stable in shape and size, whereas those of psoriasis are constantly changing over a period of weeks to months.

The lesions of parapsoriasis can occur anywhere on the trunk and proximal extremities but are most commonly seen on the abdomen, buttocks, and thighs. In women the breasts are often involved. Parapsoriasis can occur at almost any age but is most commonly seen in the mid or late adult years. The lesions are usually asymptomatic.

The evolution of parapsoriatic plaques into those of the plaque stage of mycosis fungoides is marked by a gradual thickening. Scale becomes less apparent, and the brown-red color gradually develops dusky, violaceous hues. The round or oval outline of the plaques gradually takes on a more irregular shape. Indented (kidney-shaped) and polycyclic plaques develop. During this transition, histologic evidence of lymphocyte atypicality develops and clusters of these atypical cells appear within the epidermis (Pautrier microabscesses).

With the passage of additional time, nodules begin to appear. They may arise de novo or may develop within the preexisting plaques. Ulceration of the plaques and nodules commonly occurs. This “tumor” stage of mycosis fungoides is generally accompanied by the development of lymphadenopathy and other evidence of systemic involvement.

Other Forms of Cutaneous T-Cell LymPhoma. Exfoliative erythrodermatitis can occur secondary to widespread, severe psoriasis and various forms of eczematous disease . It can also arise in a primary form in mid or late adult life as a manifestation of CTCL. This form is termed Sezary syndrome. The clinical presentation in Sezary syndrome differs from secondary exfoliative erythrodermatitis in that there is often associated alopecia, palmar and plantar hyperkeratosis, and a significant degree of cutaneous hyperpigmentation. Patients with Sezarys syndrome usually have, at the onset, evidence of systemic involvement as noted by lymphadenopathy and the presence of circulating atypical lymphocytes (Sezary cells) .

Rarely, the first manifestation of CTCL is the sudden onset of multiple large nodules. This type of presentation was previously known as d’emblee-type mycosis fungoides, now it is recognized that such nodules may be made up of” phenotypically quite varied malignant T cells. These nodular lymphomas are simply termed peripheral T-cell lymPhomas.

Course and Prognosis

Parapsoriasis is an extraordinarily stable and slow-moving disease. Gradual centrifugal enlargement of individual plaques does occur, but years go by before light microscopic and clinical evidence of malignancy is seen. Patients frequently develop other health problems and die long before mycosis fungoides becomes a problem.

The course of mycosis fungoides, once present, is extremely variable. A few patients will develop evidence of systemic disease in as little as several years, but most will go for S to 10 years before tumors, ulcers, and evidence of internal involvement develop. Once these changes occur, however, the pace of the disease picks up appreciably. At that point, the clinician can predict death from the disease within 2 to 5 years. In spite of this slow and highly variable course, one thing is clear, Mycosis fungoides is inevitably fatal. One escapes death from mycosis fungoides only by dying from some other process.

Pathogenesis

The cause of parapsoriasis and that of mycosis fungoides are unknown. A current, attractive hypothesis, however, suggests that mycosis fungoides develops as an uncontrolled immunologic reaction to a persistent antigen that is deposited on or is developed in the skin. This hypothesis, which is based on the large number of Langerhans cells present in the early inflammatory infiltrate, suggests that Langerhans cells process and convey an unknown antigen to helper T-cell lymphocytes. These T cells, in turn, activate a clone of T cells that, perhaps because of persistent stimulation, eventually develops malignant characteristics. Once formed, these malignant T cells increase in number and collect first in the skin and eventually in the lymph nodes and other internal organs. In the early lesions of mycosis fungoides the proportion of malignant to benign inflammatory cells is low. In the tumor stage a much higher proportion of malignant cells is found. The transition of parapsoriasis to CTCL is marked immunophenotypically by the gradual loss of pan T-cell antigens from the mononuclear cells that make up the “inflammatory” infiltrate in the cutaneouslesions. Evidence of clonal expansion, as measured by the presence of gene rearrangement in the T-cell antigen receptor, also gradually becomes apparent.

Discovery of the human T-cell lymphotropic virus type I and other related retroviruses has added another dimension to our understanding of cutaneous T-cell lymphomas. Infection of helper T-cell lymphocytes with this virus results in eventual clonal proliferation of infected cells. It seems likely that at first this is a latent infection that only subsequently leads to transformation and proliferation.

In any event, it is apparent that CTCL, like most other forms of malignancy, develops in a stepwise manner in which one or more mutational steps are followed by both clonal expansion and, eventually, additional mutational events.

Therapy

Patients with parapsoriasis are often first treated with topically applied steroids. Unfortunately, the degree of response is usually unsatisfactory. The next step for most patients involves the use of topically applied nitrogen mustard or the administration of PUVA therapy. With either modality, approximately 80% of patients can obtain a complete cutaneous remission. These remissions usually must be maintained by continuous treatment; once therapy is stopped, relapse regularly occurs. Those who fail to respond and those who break through during treatment can be treated with electron beam radiation.

The more radical approach involves the initial use of total-body electron beam irradiation with or without additional adjuvant therapy. Complete remissions are obtained in 90% of the patients treated, and more importantly, about 20% of these patients maintain their remissions indefinitely without further therapy. Unfortunately, this approach exposes patients to a considerable amount of radiation, is time consuming, and is expensive.

Patients with evidence of systemic disease are usually given multiple-drug chemotherapy in addition to total-body electron beam therapy. Unfortunately, no matter how aggressive an approach to therapy is taken, cure is not possible in those with any evidence of systemic disease. Other treatments currently being used for CTCL include extracorporeal, photophoresis (PUVA therapy of lymphocytes) and the systemic administration of retinoids and interferon-alfa.

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1. Distribution: the groin and exposed areas of the arms and legs
2. Bacterial culture
3. Response to therapy
   

   Clinical Presentation

   The small I-2-mm pustules of bacterial folliculitis are yellow-white in color and are surrounded by a narrow ring of erythema. Those that are pierced by a hair are acuminate (pointed), those that are not are dome-shaped. Only a few pustules are present at anyone time, and there is relatively little tendency for clustering. Fever and lymphadenopathy are not seen. The diagnosis of bacterial folliculitis is usually made on a clinical basis, but confirmation can tie obtained by Gram stain and bacterial culture.

Course and Prognosis

Individual untreated pustules resolve spontaneously in about a week, but often as quickly as one heals, one or more new pustules appear elsewhere on the body. This spread develops as the result of external inoculation via the fingernails. Hematogenous spread does not occur. On rare occasions bacterial folliculitis leads to deeper infection such as cellulitis or furunculosis.

Pathogenesis

Bacterial folliculitis usually represents infection of the upper hair follicle with Staphylococcus aureus. Streptococci also are occasionally found, but they rarely if ever are the inciting organism. A few cases of Pseudomonas sp. folliculitis have been reported. This uncommon and, often, rather severe type of folliculitis occurs as a result of contaminated water in hot tubs. Minor skin trauma of various sorts probably plays a role in the development of all types of bacterial folliculitis.

Therapy

Topical antibiotics may be used if only one or two pustules are present. Systemic antibiotics are preferred for patients who have a large number of lesions or who have problems with recurrent lesions. Some of these latter patients will be found to be staphylococcal carriers.

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1. Distribution: trunk, but palm and sole involvement IS characteristic when present
2. Target lesions
3. Papules and plaques are similar but less transient than those in urticaria

Clinical Presentation

Erythema multiforme is characterized by the presence of flat-topped, sharply marginated papules 1 to 2 cm in diameter. The color is generally duskier than the hright red of urticarial lesions. Typically, at least a few of the larger papules will be of the target type in which three concentric rings are found: an outermost red ring, a lighter-colored intermediate ring, and a central, dusky-colored bull’s-eye. Bullous changes, when they are present develop from the center of such lesions. The lesions of erythema multiforme seem to exist on a spectrum with those of urticaria. They differ from urticarial papules by being considerably less transient (they change in days rather than hours), by being a duskier red (less edema to “dilute” the redness), and by showing less tendency for coalescence and serpiginous outlines.

The lesions of erythema multiforme may occur anywhere on the body, but the presence of lesions on the palm and sole is quite characteristic. A search should be made for mucosal lesions, since the presence of such lesions may presage the development of Stevens-Johnson syndrome. The amount of pruritus that accompanies erythema multiforme varies from minimal to moderate. It is usually less troublesome than that which occurs in urticaria.

The diagnosis of erythema multiforme is made on the basis of clinical examination. Biopsies can be used to support a clinical diagnosis.

Atypical clinical Presentatians. Many patients present with a condition that exists between urticaria and erythema multiforme in clinical appearance. The flat-topped papules are bright red and show some tendency for coalescence. Unlike the lesions of urticaria, however, once present they remain unchanged for days. On the other hand, target lesions are not present, and mucous membranes are not involved. Such a picture is hardly multiform.

Erythema multiforme occurring with bullous changes, mucous membrane involvement, and fever is known as the Stevens-johnson syndrome . The etiology and pathogenesis are the same as for conventional erythema multiforme, but morbidity is considerably greater.

Toxic epidennal necrolysis of the Lyell type is a variant of erythema multiforme in which blister formation is tremendously extensive; sheets of skin lift off as might occur in a severe thermal burn. The clinical presentation is somewhat similar in appearance to that of the staphylococcal scalded skin syndrome (toxic epidermal necrolysis of the Ritter type), but the histologic site of blister formation is different, and there is considerably greater morbidity with the erythema multiforme variant.

Course and Prognosis

Most cases of erythema multiforme continue at an active level for 10 to 15 days, after which slow, spontaneous resolution occurs. Postinflammatory pigmentation may be left at the site of some lesions. Recurrent episodes are not common, except when the process is triggered by herpes simplex infections. Controversy exists as to whether or not a chronic, persistent form of erythema multiforme exists, but in most instances immunofluorescent studies suggest that “chronic” erythema multiforme is actually one of the immunobullous diseases such as pemphigoid.

Morbidity in erythema multiforme varies considerably. Few systemic symptoms and signs occur in most cases, but patients with Stevensjohnson syndrome and toxic epidermal necrolysis are quite ill, and death can occur.

Therapy

The lesions of erythema multiforme respond poorly to therapy . Patients with the more severe forms of the disease are usually treated with systemically administered steroids, but proof of efficacy and, for that matter, proof of safety are lacking. Milder cases do not require steroid therapy. Orally administered antihistamines may be of help when itching is a problem, but they will have little or no effect on the lesions themselves. Topical applications, including topically applied steroids, are not effective.

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1. Distribution: areas of solvent exposure or maceration (weak irritant), areas conforming to patient history of specific contact (strong irritant)
2. Discontinuation of exposure leads to improvement

Presentation

The relatively common problem of irritant contact dermatitis occurs because of environmental damage to the outer layers of the epidermis. Two types of irritant contact dermatitis are recognized that resulting from strong irritants and that resulting from weak irritants.

Strong-irritant contact dermatitis occurs after a single exposure and a short latent period. Because of the direct connection between the exposure and the reaction, patients can usually identify the cause with little difficulty. Examples of strong irritants include chemicals that markedly change pH (acid and alkali “burns”) or temperature (thermal burns and frostbite). Sunburn can also be conceptualized as a strong-irritant contact dermatitis, The reactions caused by strong irritants are characterized by inflammation, pain, and epithelial disruption. The latter often occurs in the form of skin necrosis. The relative lack of pruritus and scale formation often results in an appearance that meets the morphologic requirements of the eczematous group only because of fissuring and other erosion formation.

Weak-irritant contact dermatitis requires multiple exposures and, consequently, is associated with a long latent period. Because of this latency, the connection between the exposures and the reaction is often not apparent to the patient.

Fortunately, only one environmental modification (that of a change in moisture content of the skin) accounts for the majority of problems. This change in moisture content results in skin that is too dry (xerosis) or too wet (maceration). Thus, on the one hand, solvents (of which detergents and hot water exposure are the most common) dry the skin by removing the lipid layer on the outer surface of the epidermis. Without a normal lipid layer the superficial epidermal cells lose moisture because of evaporative loss, and the cells then shrink in size. This shrinkage leads to cell separation with resultant cracking and fissuring. When the fissures are very shallow and are noninflammatory, the process is known as chapping or xerosis. When the fissures are deeper and are accompanied by inflammation, the process is appropriately called irritant contact dermatitis or xerotic eczema.

Weak-irritant contact dermatitis is associated with dusky redness and mild to moderate scale formation. The skin looks taut and shiny; it feels dry and rough on palpation. Weeping, crusting, and excoriation are usually not prominent.

Irritant contact dermatitis from solvent exposure occurs mostly on the hands. A history of excess solvent exposure can usually be elicited. Alternatively, in the process known as maceration, the constant entrapment of too much fluid (water, sweat, urine, etc.) against the skin results in over hydration, swelling, and eventually epidermal cell death.

Irritant contact dermatitis from maceration is suggested by localization of the eczematous process to the feet or to intertriginous areas. When maceration is mild and is unaccompanied by evidence of epithelial disruption, the process is known as intertrigo. When the inflammation of intertrigo is acompanied by epithelial disruption (weeping or yellow scale) the term “irritant contact dermatitis” can be used. When maceration occurs intermittently rather than constantly, the picture becomes more like that seen with excess solvent exposure. The shiny, dry, cracked appearance of the toes in tennis shoe foot” and the fingers in patients with hyperhidrosis represents good examples of this phenomenon.

The diagnosis of either type of irritant contact dermatitis is made clinically; proof of the correct diagnosis requires resolution of the disease following removal of the irritant or modification of the suspected environmental factors.

Course and Prognosis

Removal of the offending environmental irritant is usually all that is needed to end the episode of dermatitis. In most cases this is easy to do, but in other instances (notably hand eczema resulting from solvent exposure and diaper dermatitis resulting from urine retention) it may be quite difficult. In such situations the addition of topically applied steroids will also be necessary. Finally, in some cases the itch-scratch cycle will become superimposed on the irritant contact dermatitis. Failure to end the scratching results in continuation of eczematous disease, even though the environmental factors are suitably modified.

Pathophysiology

In most cases of strong-irritant contact dermatitis, damage is caused because of a direct destructive effect on the exposed epithelial cells. In weak-irritant contact dermatitis the damageis done more indirectly. Epithelial cells, like cells elsewhere in the body, require a certain moisture content for health and function. Loss of moisture (solvent action) or the presence of excess moisture (maceration) eventually results in cell death. In all instances of irritant contact dermatitis, epithelial cell death leads to exposure of cutaneous nerve endings and the conveyance of burning, tingling, or itching to the central nervous system. If the itching sensation is translated into scratching (such as often happens in atopic individuals), prolongation and worsening of the epithelial damage can be expected.

Weak-irritant contact dermatitis, is most often caused from excess exposure to the solvent action of soap and water. Our hands will generally tolerate about 5 soap and water exposures! day. Five to ten exposures will result in mild chapping that can be controlled by lubrication. More than 10 exposures!day (a level frequently reached by housewives and mothers) will result in more severe damage, with superimposition of inflammatory changes against a background of cracking and fissuring. The skin over the rest of our body is not as resistant. Bathing twice a day leads to mild xerosis; more frequent bathing frequently results in the development of inflammatory changes also.

The deleterious effect of maceration is harder to quantitate. Skin of the groin and feet tolerates entrapment of moisture for several hours quite well, but exposures longer than this (as with chronically wet diapers or chronic hyperhidrosis of the feet) result in the appearance of eczematous disease.

Less often, weak-irritant contact dermatitis develops as a result of direct, repetitive mild trauma. Thus, constant handling of rough materials, such as stone or brick, or repeated wiping of the hands because of wet work will eventually cause the hands to become eczematized. This trauma causes direct damage to epithelial cells, but it also causes removal of the protective lipid layer, as occurs in solvent exposure.

Therapy

The first step in the treatment of contact dermatitis is the removal of the offending contactant. Of course to do this, the correct contactant must be identified. In instances of irritant contact dermatitis this is generally not too difficult, since a reasonably accurate history regarding solvent exposure, moisture entrapment, and mechanical trauma can usually be obtained. In an industrial setting this may be somewhat more difficult, but even here the number of possible solvents can usually be narrowed down to a few prime suspects.

In all instances the use of soap and detergents should be minimized. Bath oils or Cetaphil can be used instead of soap and washing, and the skin can be patted, rather than rubbed, dry. The temperature of wash water can be decreased. In situations of maceration, wet clothing (stockings, diapers, etc.) can be changed frequently and nonporous items of clothing made of nylon, plastic, or rubber can be avoided.

Once the environment has been modified, the second step is to restore a protective lipid layer. This is carried out through the application of lubricants as these emollients need to be applied frequently (4 to 6 times/ day), but some care should be taken in treating intertriginous areas such that excess sweat is not trapped.

Topically applied steroids may or may not be necessary. Generally, if itching is present or if more than a minimal degree of inflammation is present, their use is desirable.

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1. Distribution- face, neck and sun-exposed areas of the upper trunk and arms
2. Sunlight sensitivity

Clinical Presentation

Lupus erythematosus (LE) is a disease that has a very broad spectrum of clinical symptoms and signs. The spectrum is continuous, but it is convenient to consider four points on the spectrum as if they were four separate conditions.

Only the discoid-type skin lesions possess all of the characteristics of papulosquamous disease. The skin lesions that occur in patients with systemic disease lack one or more papulosquamous characteristics and thus overlap morphologically with diseases of the vascular reaction and eczematous disease groups.

The lesions in all types of LE are, in general, correlated with sunlight exposure. They are primarily found on the sun-exposed portions of the body, and in many cases the patient will have noted the development of new lesions (or the worsening of old lesions) following one or more episodes of sunlight exposure. Nevertheless, a specific history of photosensitivity is often lacking.

The patches and plaques of LE are generally asymptomatic, but a sensation of swelling and burning is sometimes described by patients with the lesions of systemic LE.

The diagnosis of LE involving the skin is often possible on the basis of clinical examination. Confirmation should be obtained through biopsy, however. Biopsy of skin lesions for direct immunofluorescence (the lupus band test) is particularly helpful, since it regularly reveals the deposition of complement and immunoglobulin at the dermal-epidermal junction. Similar deposits can also be identified in the nonlesional skin in about 70% or 80% of those patients who have systemic disease. Serologic tests for fluorescent antinuclear antibodies (FANA) are also useful in the diagnosis of LE.

Discoid Lupus Erythematosus

The skin lesions of discoid LE consist of sharply marginated, erythematous plaques 1 to 4 cm in diameter. Large lesions are often annular with a thin erythematous scaling border surrounding a white, scarred center. Smaller lesions are solid (as opposed to annular) that-topped papules and plaques diffusely covered with scale. lesions of discoid LE occur anywhere on the face but are most often found on the lateral cheeks, particularly at the Lawline. The distribution, although usually bilateral, is often not symmetrical. Lesions in the scalp occur as sharply localized patches of hair loss . Gray-white plaques are sometimes found on the lips and oral mucous membranes. Discoid LE occurs with approximately equal frequency in men and women. The disease develops at any point from childhood to late adult life . Systemic symptoms and signs are almost always absent in patients with discoid lesions. The incidence in men and women is almost equal. Antinuclear antibodies as determined by fluorescent antinuclear antibody (FANA) tests are usually negative.

Disseminated Discoid Lupus Erythematosus

There is, however, less tendency for central clearing and for scarring. Moreover, the distribution pattern is more extensive; lesions are found on the sun-exposed surfaces of the arms and hands as well as on the face. Scarring alopecia is not often present. Ten percent to 20% of patients with this type of LE will have a positive F ANA test.

Subacute Lupus Erythematosus

Often, the term subacute cutaneous is used for this type of disease. Two types of lesions may occur. The first consists of lesions that are annular plaques 2 to 10 cm in diameter. The ring of the annulus is 3 to 5 mIll wide and has little or no scale. The central portion appears as normal skin. Coalescence of these lesions to form larger plaques with a gyrate configuration sometimes occurs . The second type consists of solid plaques that resemble psoriasis. Differentiation from psoriasis is possible because the margination may be a bit less distinct, the scale size is smaller, and there is no evidence of the Koebner phenomenon. Both types of subacute LE are distributed primarily on the upper trunk and lateral arms; the face is usually spared. Patients with subacute LE usually have a positive FANA test; more specifically, Ro (SSA) antibodies are regularly present.

Acute Systemic Lupus Erythematosus

The cutaneous hallmark of acute systemic LE is the presence of symmetrical, poorly marginated, erythematous plaques on the upper malar prominences. The bridge of the nose may also be involved. Scale formation in this so-called butterfly eruption is minimal, and the plaque is usually somewhat edematous. When lesions occur other than on the face, there is a marked tendency for coalescence, as opposed to the smaller discrete lesions of discoid LE. Hair loss, when it occurs, is diffuse rather than localized. Mucous membrane lesions occur in about 25% of patients, they are identical with those seen in discoid LE .

Both sides of the hands are regularly involved. Small patches of erythema are located on the dorsal surface of the phalanges, but the area over the knuckles is spared. Reddening and telangiectasia are frequently present in a narrow band at the posterior nail folds. The palmar surfaces of the hands are often violaceous. This color change is particularly notable over the tips of the fingers and on the thenar and hypothenar eminences. Small, bright red, blanching macules or pinpoint violaceous vasculitic lesions may be superimposed against these duskier color changes. Women with this condition outnumber men with this condition by a considerable margin .

Course and Prognosis

The course and prognosis of LE correlate rather well with various types of cutaneous lesions. Patients with discoid lesions confined to the face may have a few minor laboratory abnormalities but rarely, if ever, have symptoms and signs of systemic disease. Moreover, 95% of such patients will have a normal life span with only cutaneous morbidity as a manifestation of their disease.

Patients with disseminated discoid skin lesions usually have a number of minor laboratory abnormalities, but they, too, rarely develop significant systemic disease.

Patients with lesions of subacute LE often have fever and arthralgia, but cardiac, central nervous system, and renal involvement are usually mild or absent. Patients with lesions of acute LE are highly likely to have serious systemic symptoms and signs.

The lesions of discoid LE heal with scarring and sometimes “burn out” altogether after 10 to 20 years of activity. The lesions of subacute and acute LE heal without scarring. These latter lesions tend to mirror the activity of the underlying systemic disease; i.e., they fade during periods of remission and reappear during exacerbations.

Pathogenesis

The cause of skin lesions in LE is not known. In most instances, sunlight seems to play an important precipitating role. Exposure to the 280- to 320-nm wavelengths of ultraviolet light (the UVB, or sunburn, spectrum) presumably leads to DNA damage in epithelial cells. It is hypothesized that this modified DNA then acts as a new antigen that stimulates the production of “autoimmune” antibodies. The production of these antibodies by B cells may be enhanced by a reduction in suppressor T cells. Antibodies, once formed, are deposited along with complement in the skin and other organs. Genetic factors, as manifest by the frequency of familial cases and the presence of certain HLA patterns, are undoubtedly important. Since the more serious forms of LE occur primarily in women, it is suspected that the presence of estrogens (or absence of androgens) may playa role.

Therapy

All patients should be protected from ultraviolet light irradiation in the UVB (sunburn) spectrum. This can be accomplished rather well by regular application of sunscreens with a high sun protective factor (SPF) . In addition, protective clothing and a change in lifestyle that moves outdoor activities to the beginning and end of the day are recommended.

The cutaneous lesions of LE resolve with steroid treatment. Discoid lesions respond inconsistently to topical steroids but do improve with intralesional injections of triamcinolone. The lesions of subacute and acute LE clear if associated systemic disease is treated with systemic steroids. The oral administration of hydroxychloroquine (Plaquenil) in a daily dose of 200 to 400 mg is very helpful in the treatment of all types of lesions

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This secondary eczematization is particularly likely to occur with psoriasis, dennatojhyte fungal disease, and candidiasis. In situations such as these, the process involved is very much. Analogous to the development of stasis dermatitis in patients willI stasis and to the development of dyshidrotic eczema in patlients with dyshidrosis.

Dennatitis hepetiformis, like scabies, represents a special use. Both of these conditions, though basically vesicular in nature, are so severely pruritic that they are virtually always excoriated and eczematized. Thus, though scabies and dermilitis herpetiformis are listed in both the vesiculobullous group and the eczematous group, they will present as eczematous diseases about 95% of the time.

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