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New ScratchMeNot Colors Raise Awareness During National …

According to research, approximately 10 percent of children suffer from eczema, usually starting in infancy, a skin condition that constitutes an itchy rash. Many children cannot stop scratching long enough for their skin to heal. That is why ScratchMeNot Flip Mitten Sleeves are essential for young ones with eczema, for newborns to age 6.

In recognition of National Eczema Month (October), ScratchMeNots have unveiled two new colors, Papaya Splash and Puzzled Green. The colors coordinate with the National Eczema Association’s brand colors and work to increase awareness about the prevalence of eczema and ways to help ease its effects.

Andrea Thomas, creator of ScratchMeNots, is excited about the new colors and the chance to raise awareness. “Our children wearing NEA colors can help spread the word by educating those we encounter about eczema and how it impacts children and families,” she said. “Plus, the colors are great and can easily be worn with Halloween costumes.” Puzzled Green; think Incredible Hulk.

“With eczema, kids are constantly scratching itchy skin which causes skin damage rather quickly. We’re excited that ScratchMeNot Flip Mitten Sleeves prevent this damage by allowing parents to cover their fingers when they scratch and when the scratching has subsided, parents can open the mittens allowing hands free time,” said Thomas. When their hands are covered, children can still do all normal activities including playing, eating and writing.

Eczema Awareness Month is all about education, informing the public about what eczema is, how to treat it and raising support for continued research. Throughout the month of October, ScratchMeNot is offering $5 off of their Day & Night Duo Pack (coupon code: SMN5RP) or 20 percent off three or more ScratchMeNots (no code needed).  Visit to purchase and learn more about product benefits and initiatives.

To learn more about eczema, visit the National Eczema Association’s website. Andrea Thomas, the creator of the ScratchMeNot, can be reached for comment at 888.220.9026.

About ScratchMeNot

According to research, approximately 20 percent of children suffer from eczema, usually starting in infancy, a skin condition that constitutes an itchy rash. Many children cannot stop scratching long enough for their skin to heal. That is why ScratchMeNot Flip Mitten Sleeves are essential for young ones with eczema, for newborns to age 6.

Quickest Eczema On Hands Natural Cure Review In Smithtown


Quickest Eczema On Hands Natural Cure Review In Smithtown

Quickest Eczema On Hands Natural Cure Review In Smithtown

Quickest Eczema On Hands Natural Cure Review In Smithtown

Quickest Eczema On Hands Natural Cure Review In Smithtown Quickest Eczema On Hands Natural Cure Review In Smithtown Quickest Eczema On Hands Natural Cure Review In Smithtown

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Noneczematous Contact Dermatitis – Hindawi Publishing Corporation


Irritant or allergic contact dermatitis usually presents as an eczematous process, clinically characterized by erythematoedematovesicous lesions with intense itching in the acute phase. Such manifestations become erythematous-scaly as the condition progresses to the subacute phase and papular-hyperkeratotic in the chronic phase. Not infrequently, however, contact dermatitis presents with noneczematous features. The reasons underlying this clinical polymorphism lie in the different noxae and contact modalities, as well as in the individual susceptibility and the various targeted cutaneous structures. The most represented forms of non-eczematous contact dermatitis include the erythema multiforme-like, the purpuric, the lichenoid, and the pigmented kinds. These clinical entities must obviously be discerned from the corresponding “pure” dermatitis, which are not associated with contact with exogenous agents.

1. Introduction

Allergic contact dermatitis (ACD) is a common cutaneous eczematous disorder caused by contact (either direct or aeromediated) with a range of environmental substances. Pathogenetically, ACD results from an immune reaction involving both innate and adaptive immunologic mechanisms. In particular, hyperreactive response to small chemicals (haptens) penetrating the skin depends on a series of events, such as haptens capability to activate and mobilize cutaneous dendritic cells (cDC), generation of hapten-epitopes for T-cell recognition, and hapten-cDC complex ability to prime effector T cells with skin homing proprieties [13]. In sensitized individuals, skin or systemic challenge with the specific sensitizer determines rapid recruitment of effector T cells, along with natural killer lymphocytes, which mediate tissue damage through release of proinflammatory cytokines and through hapten-loaded keratinocytes killing.

Clinics of ACD are generally polymorphic. Besides the classic eczematous form, in fact, different noneczematous clinical variants are possible [1, 46]. The causes for such variability in ACD clinical aspects are many (Table 1). According to our data (unpublished), considering >30.000 patch tested individuals for contact dermatitis, noneczematous forms are slightly more common (52%) than the classic eczematous one (48%). Various clinical patterns of noneczematous ACD have been described: some are linked to topical use of specific haptens and others more often dependent on allergens systemic administration (Table 2). The most represented forms are described as follows.

2. Erythema Multiforme-Like Contact Dermatitis

Of all noneczematous clinical variants, the erythema multiforme-like (or “contact erythema multiforme”) is the most common. It can be elicited by different substances, particularly exotic woods, medicaments, and ethylenediamine (Table 3).

2.1. Causes

Woods and plants. Among exotic woods, Brazilian rosewood (Dalbergia nigra), pao ferro (Machaerium scleroxylon), and Eucalyptus saligna are relevant as occupational causes of erythema multiforme-like eruption in carpenters, foresters, and cabinet makers. Antigens in pao ferro and Brazilian rosewood are crossreacting quinones, respectively, R-3, 4-di-methoxy-dalbergione, and R-4-methoxy-dalbergione [7, 8]. Literature also lists extraoccupational cases from wooden bracelet [9] and pendants [10] made of D. nigra. M. scleroxylon has been described to cause a similar eruption in hobbyists who handled this type of wood to build boxes [11].

Other reported causes of erythema multiforme-like reactions include Artemisia vulgaris [12, 13], poison ivy [14, 15], Hypericum erectum [16], and terpenes [17]. Tincture of capsicum caused an analogous reaction in a woman who used the concoction to treat her knee arthritis [18]. Inula helenium, contained in a mixture to treat back pain, has also induced erythema multiforme-like eruption, with positive patch tests to sesquiterpene lactone mix and alantolactone [19]. Notably, Primula obconica can also induce comparable eruptions [2023]. We observed an erythema multiforme-like reaction in a plant nursery worker, who had handled plants of P. obconica. The dermatitis involved hands, forearms, and face. Patch tests were positive to primin (0.01% in pet), leaves and flower. Histology showed foci of hyperkeratotic orthokeratosis, mild spongiosis, exocytosis, and few isolated necrotic keratinocytes; at the superficial and mid dermis, a largely perivascular lymphocytic infiltrate was present [24].

Topical Medicaments. Numerous topical drugs are reported as cause of erythema multiforme-like contact dermatitis, the vast majority being antimicrobials. According to our observation, pyrrolnitrin can trigger this kind of eruption [25, 26]. Other causative drugs include sulfonamide [27, 28], promethazine [25], neomycin [25], mafenide acetate [29], ethylenediamine [25, 30], and mephenesin [31, 32]. Among nonsteroid anti-inflammatory drugs, phenylbutazone [33], bufexamac [34], and mofebutazone [35] have been reported. Among corticosteroids, budesonide [36] and triamcinolone acetonide [37] caused analogous reactions.

Miscellany. Erythema multiforme-like eruptions can be the expression of contact allergy to nickel [3841] and cobalt [39]. 9-Bromofluorene induced a skin acute reaction in several chemistry students, who were exposed to the product during its synthesis [42, 43]. Finally, many other compounds have been associated to erythema multiforme-like reactions, although exceptionally [5, 6].

2.2. Clinical Features

Early lesions are eczematous in morphology and localized at the allergen contact site. After a 1 to 15 days delay, the erythema multiforme-like eruption follows, involving the area around the original lesions or rather extending to the whole cutaneous surface. The latter occurrence generally ensues systemic exposition to drugs which the patient had previously been sensitized to topically. Target-like, erythematovesicular, or urticarial lesions are characteristic. Resolution is slow-paced; these manifestations persist usually much longer than the original eczematous lesions (or sometimes appearing after regression of the latter). Itching sensation is also typically present in polymorphic reactions [1]. Patch tests generally elicit eczematous positive reactions, with the exceptional vesico-bullous or urticarial lesions.

Differential diagnosis is set out with true erythema multiforme (Table 4), the latter showing almost all target-like lesions with typical acral distribution and crops-like onset.

2.3. Histopathology

The histology is generally aspecific. Epidermis shows spongiosis and exocytosis. Mild upper dermis edema and perivascular lymphohistiocytic infiltration are noticeable. Vacuolar degeneration of basal cells is rarely present, while epidermal necrosis is very mild or absent. When bullae are present, they are intraepidermal [1].

The histopathology of true erythema multiforme shows frank epidermal necrosis and vacuolar basal cells degeneration, while bullae are subepidermal [1].

3. Purpuric Contact Dermatitis

This particular form of noneczematous contact dermatitis is of unusual observation, and many cases remain undiagnosed. The eruption evolves in several weeks after the withdrawal of the offending agent and resolves with more or less persistent pigmentation. The purpuric aspects of contact dermatitis, and the respective patch test reactions can be secondary to irritant, or more frequently allergic, mechanisms [44].

3.1. Causes

The most frequent causative factors are listed in Table 5. Certain components of rubber and textile are recurrently reported in the literature.

Rubber. First reported cases date back to 1968: 9 women developed purpura from cloth elastic inserts; in every instance patch tests turned positive to N-isopropyl-N-phenyl-paraphenylenediamine (IPPD), a rubber antioxidant [45]. Other 2 cases, showing diffuse purpuric reactions with negative bloodwork, were associated to IPPD and specifically to the use of rubber boots [46]. Fisher reported 3 cases, respectively, from rubber diving suit, elasticized shorts, and rubberized support leg bandage; in all 3 patients patch tests turned positive to IPPD [47, 48]. The author therefore fashioned the “PPPP syndrome,” defined as an ACD characterized by pruritus, petechiae, and purpura, caused by IPPD. IPPD also prompted similar eruption in a woman in the pattern of her brassiere [49] and in a man at rubber boots contact sites [50]. PPPP syndrome has also been described following use of orthopedic elastic bandages [51] and rubber gloves [52]; in the latter case patch tests were positive not just to IPPD but to N-cyclohexyl-N′-phenyl-paraphenylenediamine and N,N′-diphenyl-para-phenylenediamine as well.

Textile. From 1969 to 1972, Osmundsen gathered 167 cases of purpuric reactions from an optical whitener contained in washing powders [53, 54]. The petechial and itchy dermatitis interested those areas which are typically subject to tighter contact with clothes (armpits, arms, upper limbs folds, neck and thighs). The offending agent was Tinopal CH 3566, a mixture of 2 noncrossreactive pyrazolines (monochlorobiphenyl-pyrazoline and dichloro diphenyl pyrazole). Tinopal CH 3566 was used to bleach nylon fibers and caused a similar epidemic outbreak in Spain, where 103 were collected [55]. From that time on, the product was discontinued with no more cases reported. As of today, risk-free stilbene-based optical whiteners are employed.

A sailor developed generalized purpuric lesion with pigmentary outcomes at sites of contact with the military blue uniform. Patch tests evidenced positive reaction to Disperse Blue 85, while histology demonstrated Schamberg disease sign [56]. We directly observed a case of purpuric ACD to Disperse Yellow 27 (Serisol Fast Yellow 6DW), an azoic dye used in acetate and polyester fibers, a result of para-aminoacetanilide and paraphenylphenol. The dye was part of a pair of trousers inner lining, and the dermatitis, while interesting the whole skin surface, started from and was particularly manifest at the thighs. Thin layer chromatography from textile extract demonstrated only one component, Disperse Yellow 27. Histology proved traditional aspects of ACD, with lymphocytic infiltrate and intense perivascular edema, associated to noticeable erythrocyte extravasation [57]. Purpuric eruptions have also been described in a black hats vendor from paraphenylenediamine [58], in British soldiers from formaldehyde resins contained in kaki wool shirts [59], and in a man assigned to mixed wool-synthetic residues harvesting [60].

Plants. Frullania induced a diffuse purpuric reaction; histology showed signs of leukocytoclastic vasculitis; however, circulating immune complex and complement deposition assays were also positive [61]. Agave americana L, of Agavaceae family, can determine purpuric contact dermatitis with histological features of leukocytoclastic vasculitis [62]. We also observed a similar case, secondary to plant latex contact [63]. Zea mais (corn) has been shown to induce irritant purpuric phytodermatitis some hours after contact to green leaves. Patch, photopatch, and scratch tests with alcoholic extracts of different plant parts (leaves, trunk, efflorescences) all resulted negative [64]. Two-hour experimental exposition to 98% d-limonene resulted in a severe and several week persistent purpuric reaction 6 hours after contact [65].

Miscellany. Fiberglass can induce direct or aeromediated contact dermatitis, with pruriginous, 0,1–0,5 mm diameter, mostly follicular purpuric papules. Exposed and nonexposed areas are both affected, since these fibers are able to pass through clothing [66, 67]. Clothes contaminated by being washed together with fiberglass curtains can also induce purpuric dermatitis [68].

Vasculitic purpuric eruptions to Peru balsam [25, 69], ethylenediamine [70, 71], benzoyl peroxide [72], and proflavine [73] have also been reported.

3.2. Patch Tests Purpuric Reactions

As is well known among those who practice dermatoallergology, petechial reactions to cobalt patch test, without edema, vesicles, and infiltration, can be observed. These are toxic in nature rather than allergic. Schmidt et al., in a 4-year time span, observed 123 cases (4.7%) of cobalt petechial reactions out of a total of 2594 patch-tested patients. Twenty-three patients were retested and developed new petechial responses in 60% of cases. Based on these authors data, the incidence of positive allergic reactions to cobalt was lower (2.9%) than the incidence of primary irritant reactions [74]. Judging on our practice, cases of petechial nonallergic reactions to cobalt and chrome are indeed rather numerous and frequently reproducible.

3.3. Clinical Features

Purpuric contact dermatitis can be either toxic or allergic in nature. From a clinical-morphological perspective, differential diagnosis is not straightforward: both present palpable purpuric elements, evolve slowly and are followed by variably intense and persistent pigmentation. At times, clinical extension represents a useful feature in differentiating the 2 forms, the irritant being strictly limited to contact sites. Moreover, lesional elements resolve more rapidly and are less infiltrated in the irritant form compared to the allergic one.

Diffuse contact irritation from fiberglass must be discerned from scabies, eczema (prurigo-like), animal and vegetal acariasis, and if persistent, from Hodgkin disease. The anamnestic data of epidemic bursts in industries or bureaus (fibers dispersed from defective air conditioners) greatly aid diagnosis [75].

The allergic form of purpuric contact dermatitis generally features diffuse and polymorphic manifestations: papulopurpuric and papulovesicular lesions parallel classic eczematous foci. The latter are limited to the original contact site with the offending noxa. Secondary distant lesions can also present polymorphic or vasculitic aspects, as we have directly observed. Purpuric patch tests reactions are obviously vesicular and infiltrated [44].

3.4. Pathogenesis and Histopathology

The pathogenetic mechanism of purpuric contact dermatitis is currently unknown. Hemostasis or complement system alterations are not generally described in reported cases nor are immune complexes commonly isolated. In every case we observed, among which 3 severe cases from Peru balsam with frankly vasculitic and bullous lesions and various cases from ethylenediamine (in which the rash had followed systemic administration of aminophylline), specific laboratory exams fell into normal range [25, 44].

Since endothelial cells degeneration is evident at electron microscopy, a selective effect on these cells has been hypothesized. In detail, specific toxic or allergic substances as well as certain mechanical stimuli (fiberglass) would exhibit an affinity for vessels endothelium [47, 57, 58]. Alternatively, a primary lymphocytic reaction in response to the antigen at the perivascular site would free toxic lymphokines, ultimately responsible of endothelial damage [72].

Histopathology has been described, with comparable results, in most reported cases. In the epidermis, spongiosis and lymphocytic exocytosis are constant features, along with possible bulla formation. In the upper dermis the signs of leukocytoclastic vasculitis (vessels fibrinoid degeneration, edematous endothelium, scarce perivascular lymphomonocytic and neutrophilic infiltrate, erythrocytes extravasation, and karyorrhexis) are visible. The same features are present when examining a patch test response lesion (Table 6) [47, 74].

Bloodwork, histologic and patch test examinations are valid to differentiate the condition from vascular, hemostatic, and idiopathic purpuric affections.

4. Lichenoid Contact Dermatitis

A particularly uncommon form of noneczematous contact dermatitis presents with clinical features resembling those of lichen planus. It affects both skin and mucosal membranes.

4.1. Causes

Color developers, substances derived from paraphenylenediamine, are the most common cause of allergic contact lichenoid eruption. Among these compounds, Kodak CD2 (4-N, N-diethyl-2 methylphenylenediamine), Kodak CD3 (4-N-ethyl-N-2-methanesulfonylaminoethyl-2-methyl-phenylenediamine sesquisulfate monohydrate), Kodak CD4 (2-amino-5-N-ethyl-N-(hydroxyethyl)-aminotoluene sulfate), Ilford MI 210 (N-ethyl-N (5-hydroxy-amyl) para-phenylenediamine hydrogen sulphate), and Agfa TSS (4-amino-N-diethylaniline sulfate) [75].

Other cases of lichenoid contact dermatitis have been reported by Mandel, in 9 out of 11 workers with contact allergy to a color developer [76], and by Fry in 7 out of 20 patients with analogous sensitization [77]. High speed, black-and-white film processing implies the use of similar chemicals, which can induce lichenoid reactions [78]. As a general rule, the eruption from color developers spares the oral mucosa [79]. Cases from paraphenylenediamine in hair dyes [80], P. obconica [81], nickel [82], epoxy resins [83], aminoglycoside antibiotics [84], and methacrylic acid esters for industrial use [85] have also been described. Oral mucosae involving forms are due to copper [86], zinc [87], and mercury [88] contained in dental restorations.

4.2. Clinical Features

Eczematous lesions evolve or associate with papulous lesions with peculiar lilac-red gradation. The eruption mostly involves contact sites, later widely spreading with mucosal sparing. Course is prolonged and leaves variably intense pigmentary changes lasting up to some months. Lichenoid contact dermatitis has to be differentiated from lichen planus, with its characteristic papulous polygonal lilac lesions. The onset of lichenoid contact dermatitis is almost invariably acute and the eruption spreads rapidly. Frankly eczematous lesions at the primitive site are noticeable in many cases.

Positive reactions to patch tests are eczematous in nature, but might turn lichenoid.

4.3. Pathogenesis and Histopathology

Pathogenesis of contact lichenoid dermatitis is unclear. Systemic absorption of offending agents can elicit skin lesions far from the original site of contact. In 5 cases we observed (3 from color film developers and 2 from paraphenylenediamine), histology displayed lack of hypergranulosis, foci of moderate spongiosis, and focal basal stratum vacuolization. A patchy mononuclear infiltrate was evident in the upper dermis [86]. Basal cell vacuolization is the cause of incontinentia pigmenti, which could explain skin lesions peculiar color, a blend of red from flogosis with blue from dermal melanin. Table 7 compares the different histopathological characteristic of lichenoid contact dermatitis and lichen planus.

5. Lymphomatoid Contact Dermatitis

This uncommon dermatitis manifests with the clinical features of plaque parapsoriasis or an early stage mycosis fungoides [1, 70]. There are no specific causing haptens [8995], the most frequently reported being paraphenylenediamine, para-tertyl-butyl phenol resin, gold, ethylenediamine, and nickel. Patch test reaction to these is eczematous in nature and can persist for several days. Lymphomatoid contact dermatitis and mycosis fungoides alike present with infiltrative patches; the former, however, demonstrates a bright erythematous color and undefined margins.

Histology is crucial in differentiating the above two conditions. Spongiosis is much clearer, and exocytosis is typically lymphocytic in contact dermatitis. Mycosis fungoides instead shows atypical lymphocytes in focal abscess-like aggregations (i.e., the pathognomonic Pautrier’s microabscesses) and a band-like subepidermal infiltration of large lymphoid cells with cerebriform nuclei (Table 8).

6. Pigmented Contact Dermatitis

Described by Osmundsen in 1970, it is a melanic primitive hyperpigmentation, usually observed in dark phototypes and mostly occupational [96]. The author observed an intense and bizarre skin hyperpigmentation due to contact with an optical whitener (Tinopal CH 3566) used in washing powders and made by a combination of two pyrazolone derivatives, as of now discontinued.

Clinically, involved sites were those of textile contact dermatitis, with brown-blue to grayish hyperchromia. The same occurred at patch test application sites. Histology evidenced melanin deposits inside and out melanophages in the upper dermis.

Pigmented contact dermatitis can also be prompted by azoic dyes. An epidemic outburst from contact to naphthol AS has been reported in a textile business [97]. Hyperpigmentation was noticeable in dark skinned individuals, while fair skinned ones showed the signs of classical eczema. Sudan I, Vacanceine Red [98], and Brilliant Lake Red R [99] are other offending colorants which have been reported. Isolated occupational cases from insoluble cutting oils [100], paraphenylenediamine [101], and other substances are also described (Table 9) [102]. Riehl’s melanosis is nowadays also considered a pigmented contact dermatitis, mostly from cosmetic sensitizing fragrances and chemicals [103].

7. Pustular Contact Dermatitis

Pustules are usually associated with irritant reactions. Nevertheless, allergic pustular reactions are known from nitrofurazone [104], black rubber [105], and minoxidil [106]. The latter has been described in a woman who developed a vesicopustular eruption on the forehead after applying 2% minoxidil solution. Histology showed perifollicular lymphocytes, histiocytes, and eosinophils. Patch test response was erythematovesicopustular. Patch test was strongly eczematous in another case of pustular allergic contact dermatitis from isoconazole nitrate [107].

The implication of such rare pustular reactions remains uncertain. Pustules are sterile and transient and can displace subcorneally, as observed in a case from trichloroethylene [108].

7.1. Pustular Patch Test Reactions

Pustular reactions to contactants are frequently observed in patch test reading. Hjorth stated that atopics are predisposed to such reactions [109]. Metal salts, particularly nickel, copper, arsenic, and mercury represent the most common causes of these reactions, which are irritant in nature [110, 111]. As a matter of fact, pustular responses to nickel patch test are widely observed when testing atopics on lesional skin, with follicular papules, erythema, or lichenification [112]. This further supports the irritant nature of the phenomenon.

In subjects affected by atopic dermatitis, we often observed such pustular follicular reactions when patch testing with nickel but also with potassium bichromate. Pustules are always sterile, dry promptly, and resolve rapidly. Erythema is mild and the reaction is not pruriginous. Histology, documented in various cases, has always evidenced intraepidermial aggregations of neutrophils, without signs of lymphomonocytic exocytosis or spongiosis. We have always considered these reactions we directly observed irritant in nature [113, 114].

8. Dyshidrosiform Contact Dermatitis

Certain authors include this condition among noneczematous allergic contact forms [6]. In our opinion, this dermatitis retains frankly clinicohistologic eczematous aspects, and a proper differential diagnosis would have to be made with the endogenous eczema pompholyx. As per our observations, dyshidrosiform allergic contact dermatitis can be primitive or secondary [70, 115, 116]. The latter is defined as a contact sensitivity which complicates a preexisting primitive palmoplantar pompholyx. The latter tends to a chronic recurrent course, thus constituting a predisposing factor to occupational and extraoccupational contact allergy [117, 118]. From studies we carried out on 354 subjects with pompholyx genuine lesions, observed during a 5-year period, incidence of relevant positive patch tests reactions was 29.6%. Topical medicaments (used to treat the original pompholyx) and other substances among which paraphenylenediamine (31.5% positive reactions), chrome (25%), cobalt (10.2%), mercaptobenzothiazole (9.3%), nickel (6.5%), and para-tert-butylphenol formaldehyde resin (2.7%) were the most often implicated haptens. Patch tests relevance was related to specific occupational activities, use of peculiar gloves rather than shoes [115]. More recently, a study we conducted on 45 individuals affected by palmoplantar pompholyx confirmed an ACD incidence of 31% [116].

Primitive dyshidrosiform ACD is instead an expression of systemic contact allergy, of common observation in nickel sensitized patients. Oral challenge test with nickel reproduces the dyshidrosiform eruption in these subjects [119122], although this phenomenon has not been widely confirmed [123, 124].

Table 10 designates differential diagnosis between dyshidrosiform ACD and pompholyx. Intense erythema and constant hand dorsum involvement in the former represent useful discerning characteristics. Histologically, spongiosis and exocytosis are much more marked in ACD than in pompholyx.

Understanding The Symptoms Of Skin & Scalp Eczema | Curly Chic

Eczema is a group of chronic skin disorders that affect the hands, scalp, face, back of the neck, and skin creases of the elbows and knees. It can run in families, but it may occur for no known reason or be caused by an allergic reaction to certain foods, clothing, lotions, soaps, plants, or topical medications.

Signs and symptoms of eczema may include itching, small bumps that look like blisters, and thickened and scaly skin.

Eczema can be treated with preventive measures and medicines. The goals of treatment are to ease symptoms, especially itching, and to control the rash.

Source: Tukka Naturals


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Severe 'eczema' on hands? | diseases

7.Dyshidrosis. (pomphylox, the id reaction, chronic hand eczema, dyshidrotic eczema) Google images and …… does it look like this?

It is allergy to a dermatophyte, which is any kind of skin loving ‘bug’. Mold, yeast, bacteria, virus, parasite, pollen. It could be anywhere on or in your body. The rash on the hands(or feet) is just a red flag. Take anti-histamines for immediate relief. Fexofenadine 180mg, and 8 hours later 60mg, then every 8 hours 60mg. (Allegra to Americans and Sanofi-Aventis give out samples if you ask nicely) This is not the cure. But it will stop the itching. Go to dyshidrosis@yahoogroups for more information. http// (my website).

This condition is your immune system over-reacting to the presence of a dermatophyte.

The most common dermatophyte is Candida in its dimorphic, mycelial form in the intestines. Which is often diagnosed as Irritable Bowel Syndrome. (IBS)

The cure is really simple, but I very much doubt you can get your doctor to prescribe it for you.

You need a two week course of NYSTATIN by drops, 2 million units daily. That is 5 drops 4 times a day: then a 2 week break, then repeat. If this does not work (and I would bet the cost of your doctor visit it does.) you need a drug called Toctino, to be taken for 90 days. This is expensive, and not great for your liver, you will find a cheaper way on the links at

I am studying this condition, also called the ‘Id reaction”. Can I ask you to tell your doctor to refer to page 651, chapter 17 in the 1st volume of the Textbook of Dermatology by Rook, Wilkingson and Ebling.?

You have to realize this is NOT contact dermatitis, and it is not eczema This is a special sort of allergy, and must NOT be treated with steroids and cortisone creams and injection at all. This makes it spread..

All the creams you put on your hand will do nothing for the cure of the condition, but soaking your hand in warm water and vinegar will neutralize the histamine and give you a couple of days relief from itching until the histamine builds up again. Neuragena Norwegian Formula glycerine cream under cotton gloves at night is the least irritant.

Some people find bleach baths help, same applies, neutralizes histamine. But also reduces the fungal load on the skin, and if your dyshidrosis is caused by a seasonal airbourne mold, this is the best treatment.

Podiatrists see a lot more of this condition in response to Tinea, which is athlete’s foot. MD doctors have only out of date treatments and it is a dogma that steroids will take down the inflammation. True, but they cause the spread to new histamine receptors. In fact, it is my theory that steroid/hormonal changes, ie puberty, the pill, pregnancy and pumping iron and the peri menopause which are all hormonal/steroid changes are the inciting cause for the yeast Candida Albicans to morph into the opportunistic pathogen of the mycelia form. This is why it is not detected on allergy tests. Everybody has Candida, but not everybody has candidiasis. Only the mycelial form of Candida seems to cause the major histamine reaction which is Dyshidrosis

Patient Questions:

Do you have any symptoms of IBS?

Do you have athlete’s foot? Ringworm? Any persistent fungal or bacterial infection?

Are you on the Pill? (or HRT)

Did you take a course of steroids or antibiotics at about the time the condition started? (prescribed or not…)

Thinking back to when this started: Did you move to a new house? Area? Or a new job? Was it moldy?

Were you trying to get pregnant? pregnant? just been pregnant? breastfeeding?

Thinking back to when this started: did you have a stomach upset that persisted, did you suddenly become ‘intolerant’ to food that had previously not caused you any problems.

Can you add any information about the starting point of the condition? (Hospitalized, new relationship, rash, holiday, stress)

The hidden dangers of deodorant sprays: Headaches, eczema …

  • Inhaling large doses of chemicals from deodorant aerosols can be fatal
  • Canister fumes may cause skin reactions, allergies and heart problems
  • Teenage boys are particularly in risk zone due to common over-use

Walk past a teenage boy and you’ll almost certainly be left with the lingering smell of spray deodorant – 50 per cent of children now use deodorant by the age of 11, according to one survey, with self-consciousness about body odour often spurring them to spray to excess.

For most teenage boys, only the market leader Lynx will do.

Thanks to its insistent marketing campaigns – including the slogan: ‘Get the look that gets the girl’ – the deodorant is the world’s best-selling male grooming product, sold in 60 countries and boasting eight million users in the UK alone.

The primary target for spray deodorants is thought to be 13 to 18-year-olds, with mums the main buyers, according to Marketing Magazine.

So powerful is its hold on the teen market that some teachers have gone on to online forums to complain about ‘the Lynx effect’, sharing anecdotes about having to teach through the fug of deodorant.

But some experts are concerned teenagers are over-using deodorant, warning that inhaling chemicals from the aerosols may cause allergic skin reactions, asthma and breathing difficulties.

In very rare cases they may even trigger fatal heart problems.

Maureen Jenkins, director of clinical services at Allergy UK, says: ‘Around one in three adults in the UK have some form of allergic disease – asthma, rhinitis or eczema – and their symptoms are easily aggravated by perfumed products and exacerbated by aerosol chemicals.

‘Even people without allergies can be sensitive to chemicals found in cleaning products or toiletries, experiencing skin reactions, breathing difficulties, nausea or headaches. The reactions are made worse when it is an aerosol as the fine mist is easily inhaled.’

Dr Peter Dingle, an environmental scientist and consultant toxicologist based in Perth, Australia, says: ‘The labels on deodorant aerosols instruct you not to use them in a confined space, but I think it’s safe to say most people in the UK aren’t going to go outside to spray on their deodorants.

‘They would do it in the bathroom, most likely with the door closed – and that’s a confined space.

‘In the middle of winter, you’re not even going to have a window open. If you watch a deodorant advert, the young man usually sprays himself all over his body, which is exactly what the can tells you you’re not supposed to do. Self-image and smelling right is all important for young men and there’s a lot of peer pressure to use these products.’

This is something the Capewell family will be reminded of for the rest of their lives. Jonathan Capewell was just 16 when he died of a heart attack in the bedroom of his home in Oldham, Greater Manchester. His 17-year-old sister, Natalie, raised the alarm after finding her brother lying lifeless on his bedroom floor.

‘When we arrived at the hospital, they were still trying to revive him,’ recalls his father Keith, 58. ‘But about ten minutes later they said he was gone.

‘We were shocked. There had been no warning. They asked if he had a heart condition but there was nothing like that. He was a perfectly normal, healthy boy.’

A post-mortem examination showed Jonathan had ten times the lethal amount of butane and propane in his blood. The gases are used as aerosol propellants and it seemed they had built up in his body over many months.

At first, it was feared Jonathan had been engaging in solvent abuse – inhaling aerosol solvents to obtain a ‘high’ – but it seemed out of character to all who knew him. Keith says: ‘The coroner’s investigator checked the aerosols we had in the house but found none of the signs of solvent abuse. He came to the conclusion that Jonathan wasn’t abusing.’ The investigation turned to Jonathan’s use of deodorants.

‘He was 16 and his body was changing,’ says Keith. ‘He was starting to sweat more and worry about how he smelled. It wasn’t unusual for him to have two or three showers a day.

‘Afterwards he would spray deodorant all over his body, even in his hair, and the bathroom was the smallest room in the house. He was a bit obsessive and would have up to six different types to choose from, including Lynx. Sometimes we could smell the deodorant downstairs and we’d joke: “Are you spraying that up there or eating it?” ’

The coroner, Barrie Williams, ruled that Jonathan’s death was accidental, saying: ‘The 16-year-old was a normal, healthy teenager who was simply overcome by excessive use of antiperspirants.

‘There was an exceptionally high use of deodorant for personal hygiene. It was used in a fairly confined space against the advice of the canisters.’

But how could accidentally inhaling aerosol chemicals cause death?

Jonathan Clague, a consultant heart specialist at the Royal Brompton Hospital, says: ‘The main cause of death is usually suffocation, known as hypoxia. If oxygen is not being breathed in and something else is inhaled, such as chemicals, then suffocation occurs and the heart stops.’

After the inquest in 1998, Keith and Louise struggled to come to terms with Jonathan’s death.

‘My daughter blamed herself because she was in the house when it happened, even though there was nothing she could have done,’ says Keith.

‘I went back to work as a warehouse manager after a couple of weeks but every time the phone rang my hands started shaking and I’d be transported back to that day, expecting more bad news. I had to give it up.’ It was two years before he could work again.

He adds: ‘It’s been very hard to accept – Jonathan was only 16 and hadn’t even started out in life.’

Daniel Hurley was just 12 when he collapsed after using spray deodorant in the bathroom of his home in Sandiacre, Nottingham.

He died in hospital five days later, in January 2008. The coroner told his parents Lynsey and Robert that his death had been caused by a ‘cardiac arrhythmia, exacerbated by exposure to solvents’.

It seemed Daniel had an unknown pre-existing heart arrhythmia – a heart rhythm problem – and the solvents in the Lynx aerosol he had been using had triggered a fatal collapse.

There are several warnings on the back of Lynx canisters. Users are advised to ‘use in short bursts in well ventilated spaces’, to ‘avoid prolonged spraying’ and ‘keep out of reach of children’.

The British Aerosol Manufacturers Association (BAMA) says propellants in household aerosol products have been used safely for 40 years and that 600 million aerosols are used each year in the UK.

The association carried out its own research after Jonathan Capewell’s death, but says it was ‘unable to reproduce the conditions which could lead to harmful or fatal effects from excessive spraying of aerosol products in a confined space’.

Dr Dingle says: ‘It’s not enough for the authorities to say, “It’s OK, there’s a warning on the back of the can.” If two children have died by spraying deodorant in a confined space, there will be countless more spraying the same way. Do we have to have another death before the authorities act?

‘I would advise teenagers to stick to roll-on deodorant, preferably one of the natural ones.’

The Capewells are also calling for better awareness of the risks of aerosol deodorants.

‘Our youngest son Nathan was four when Jonathan died and as soon as he was old enough to use deodorant we drummed into him that he had to open the windows and only use short bursts. He’s 20 now and he does that to this day, wherever he is,’ says Keith.

‘I’d like to see warnings on the front of the can, like there are for cigarettes and alcohol. Because we know first hand that deodorants can be just as fatal.’

Health Tip: If You Have Hand Eczema – MedNews provides accurate and independent information on more than 24,000 prescription drugs, over-the-counter medicines and natural products. This material is provided for educational purposes only and is not intended for medical advice, diagnosis or treatment.

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Study identifies dermatitis risk for cleaners |

New Zealand’s first ever study of occupational dermatitis in cleaners has found rates of eczema among them nearly twice that of people not exposed to cleaning agents.

Centre for Public Health researchers from Massey University’s College of Health measured work-related skin symptoms in 425 cleaners involved in cleaning hospitals, tertiary institutions, schools, commercial buildings and the meatworks industry. Their results were compared with those of non-exposed workers from the retail and clerical sector as well as bus drivers.

Lead research investigator and centre director Professor Jeroen Douwes from Massey’s Wellington campus, says while the research focused on a non-life threatening affliction, the implications were still significant for the more than 30,000 cleaners employed in New Zealand.

“In terms of occupational disease it’s something that gets ignored because it’s not life threatening but it is more problematic than people realise and can really affect their ability to perform their jobs.”

The researchers found that of the surveyed cleaners 14.8 per cent reported experiencing eczema in the three months preceding the surveyed period, compared to 10 per cent of non-exposed workers – representing an almost two-fold increased risk of eczema. It was also more common for cleaners (17.6 per cent) to develop eczema in adult life compared to people not employed in the role (11.4 per cent).

Professor Douwes says cleaners were also more than twice as likely at 11 per cent to report having an itchy skin rash on their hands wrists and forearms compared to 5.3 per cent of the general population.

Overseas, occupational dermatitis is associated with work absenteeism, disability, increased use (and therefore increased cost) of medical care and pharmaceuticals and reduced quality of life and increased stress in individuals with these conditions.

The New Zealand research suggested that cleaners were incorrectly applying anti-dermatitis creams and aggravating existing conditions by re-using old gloves, sometimes for days on end rather than throwing them out, thus damaging the protective skin layer making it more vulnerable to chemical exposure.

In some cases the research revealed that cleaners were not even aware of the cleaning agents they were using and simply identified which was the correct one by the colour of the bottle.

Professor Douwes says workplaces had to accept responsibility for making cleaners aware of the products being used and give them more information about means available to protect their hands and forearms.

“Employers need to make available sufficient gloves and also provide creams and introduce preventative programmes to stop it [the onset of occupational dermatitis] happening in the first place,” he says.

The study was funded by the Department of Labour (now with the Ministry of Business, Innovation and Employment) and the Health Research Council of New Zealand.

Tips to avoid hassle eczema in hands |


The hand eczema is characterized by itching, dryness and redness. Apart from unsightly dermal This condition is very embarrassing for patients.

To prevent or minimize the symptoms of eczema you :

Keep your hands as drier is to prevent exacerbations.

When you wash your hands Use a gentle cleanser without fragrance and water is always warm.

then to wipe gently and always apply a moisturizer.

When eczema is Resurfacing avoid using hand sanitizer.

Protect hands while wearing gloves when doing housework and garden or cook.

Do not wear rings or other jewelry in your hands when you wash or do housework.

Wear waterproof gloves when you wash your hair or bathe .

Put Prolipsis in life and … changed!!