Eczematous Skin Eruptions Research Articles

Nonbullous pemphigoid representing clinical manifestation as eczematous skin eruption

Nonbullous pemphigoid representing clinical manifestation as eczematous skin eruption

Meme Kanseri Tanılı Hastada Letrozol ile İndüklenen Lineer Likenoid Erüpsiyon

Letrozole which acts as an aromatase inhibitor is used in the treatment strategy for oestrogen receptor-positive breast cancer. Cutaneous adverse effects including vasculitis and erythema nodosum of letrozole have been rarely described in literature. Recently reported eczematous skin eruption due to letrozole is one of the side effects that known to be developed by this drug. To our knowledge letrozole induced linear drug eruption has not been described in previous reports. We report 52-year-old woman who had unilateral pruritic lichenoid eruption over left tight following Blaschko lines after using letrozole. Cutaneous side effects of aromatase inhibitors can be serious as progressive cutaneous vasculitis or can be presented with mild cutaneous side effects as in our case. The physicians should be aware of this benign clinical condition. The decision to discontinue medication is dependent to the knowledge of severity of the side effects.

Dubowitz sendromlu bir yenidoğan olgusu

Dubowitz syndrome was first reported in 1965 by Victor Dubowitz. Dubowitz syndrome is a rare autosomal recessive disorder characterized by microcephaly, short stature, abnormal faces, eczematous skin eruption, and mild to severe mental retardation. In this review, we describe a female newborn with microcephaly, micrognathia, high narrow, syndactyly, clinodactyly, ventricular septal defect, poor feeding and sacral dimple. Here, we heard the requirement to report this case because of rarity.

Ektoparasitosen

Ectoparasites and epidermal parasitic skin diseases are a heterogeneous group of infections of the external layer of the skin. The most common forms world-wide are scabies, lice (Pediculosis capitis, corporis, vestimentorum and pubis), tungiasis and the hookworm-associated Larva migrans cutanea. The head louse is the most widespread parasite in children in Germany. The symptoms, apart from pruritus, eczematous skin eruptions and ictus reactions of the skin, are often unspecific and many differential diagnoses must be considered. Treatment of ectoparasites includes manual procedures, such as repeated cleansing and combing out of lice-infected hair and also local antiparasitic treatment with permethrin, pyrethrum extract, allethrin and dimeticon. Lindan which has been used for decades can no longer be used in medications after 2008 after a decision of the EU Commission. Failure of treatment of head lice can be a result of errors in the treatment which favor survival of the eggs, larvae or adults. This can be a result of too short reaction times and too economical use or unequal distribution of medications, excessive dilution due to wet hair or omitting repeated treatment stages. Additionally resistance of head lice to pyrethrum is a known phenomenon and has been reported in several countries.

Shwachman-Diamond-Syndrom als Ursache eines Säuglingsekzems mit begleitender Dystrophie

Shwachman-Diamond syndrome is an autosomal recessive multisystem disorder involving an insufficiency of the exocrine pancreas and haematological problems as main symptoms. Frequently, ichthyosiform skin lesions are described but are usually not the leading symptom of the disease. We report on a 6-months-old boy suffering from ichthyosiform and eczematous skin eruptions beginning at the age of 3 months which were accompanied by failure to thrive. Because of an atopic predisposition and a sensitisation to hen's egg the diagnosis atopic dermatitis with food allergy was established. We describe the steps leading to the diagnosis Shwachman-Diamond syndrome. Shwachman-Diamond syndrome may present with skin eruptions as main symptom. A mixed clinical picture with an atopic dermatitis may occur and can aggravate skin symptoms. Additional medical problems like failure to thrive or neutropenia should lead to further diagnostic procedures to exclude Shwachman-Diamond syndrome.

Pyrexia of unknown origin in a haemodialysis patient.

The most common cause of pyrexial reactions in the haemodialysis patient remains bacterial infections. The incidence of infection is increased in the dialysis patient [1], particularly due to indwelling central venous catheters. Pyrexial reactions have been reported with microbacterial contamination of the dialysate [2], but these are now rare events, due to the regular testing of dialysate water. Occasionally, patients may react to a component in the extracorporeal circuit. These reactions vary from local eczematous skin eruptions, to a variety of systemic reactions, ranging from headache to anaphylaxis [3]. A case of recurrent intraand post-dialysis fevers is presented as a teaching case.

Properties of Circulating Regulatory T Cells Associated with Nascent IgE Responses in Children with Atopic Dermatitis

RATIONALE: Atopic dermatitis (AD) is associated with increased circulating CD25hi regulatory T cells (Tregs) which comprise CCR6+ and CCR6neg subsets. We aim to monitor Tregs in early life and identify serum cytokine patterns which predict expansion of these cells, increased total IgE levels and persistent disease. METHODS: Children (5 months to 14 years, n=13) presenting with eczematous skin eruption were evaluated for disease severity (SCORAD). Measurement of serum IgE (CAP assay) and cytokines/chemokines (27-Plex cytometric bead assay or ELISA) was performed. PBMCs were analyzed by flow cytometry for expression of surface antigens and Foxp3 protein. RESULTS: Elevated levels of factors implicated in altered Treg homeostasis or function (IL-1, IL-2, IL-6, and IL-15) were measurable in early life in a subset of children. Levels of AD-associated chemokines (CCL17 and CCL18) were highly variable in early life and, in contrast to adult patients, did not correlate with total IgE titers. Children >24 months exhibited markedly increased total IgE compared with younger children (mean=4,260 IU/ml [n=5] vs. 30.2 IU/ml [n=8]) and this reflected a shift from an IgE ab profile directed against foods, to one dominated by inhalant allergens. Evidence for expansion of CD25hi Tregs (>79% Foxp3+) was present in 2 of 3 children (ages 4 and 13 years) with moderate/severe AD, with these cells constituting 5.1% and 8.6% of total CD4+ T cells. However, the proportion of memory Tregs which expressed CCR6 was diminished compared with adults. CONCLUSIONS: Our findings demonstrate the feasibility of evaluating altered Treg homeostasis associated with nascent allergen-specific responses in AD.

Murine model of atopic dermatitis associated with food hypersensitivity

Background: Atopic dermatitis (AD) is an eczematous skin eruption that generally begins in early infancy and affects up to 12% of the population. The cause of this disorder is not fully understood, although it is frequently the first sign of atopic disease and is characterized by an elevated serum IgE level, eosinophilia, and histologic tissue changes characterized early by spongiosis and a CD4+ TH2 cellular infiltrate. Hypersensitivity to foods has been implicated as one causative factor in up to 40% of children with moderate-to-severe AD. Objective: The purpose of this study was to establish a murine model of food-induced AD. Methods: Female C3H/HeJ mice were sensitized orally to cow’s milk or peanut with a cholera toxin adjuvant and then subjected to low-grade allergen exposure. Histologic examination of skin lesions, allergen-specific serum Ig levels, and allergen-induced T-cell proliferation and cytokine production were examined. Results: An eczematous eruption developed in approximately one third of mice after low-grade exposure to milk or peanut proteins. Peripheral blood eosinophilia and elevated serum IgE levels were noted. Histologic examination of the lesional skin revealed spongiosis and a cellular infiltrate consisting of CD4+ lymphocytes, eosinophils, and mast cells. IL-5 and IL-13 mRNA expression was elevated only in the skin of mice with the eczematous eruption. Treatment of the eruption with topical corticosteroids led to decreased pruritus and resolution of the cutaneous eruption. Conclusion: This eczematous eruption resembles AD in human subjects and should provide a useful model for studying immunopathogenic mechanisms of food hypersensitivity in AD. (J Allergy Clin Immunol 2001;107:693-702.)

ALLERGIC AND NONALLERGIC ECZEMATOUS DERMATITIS

To discuss nonallergic eczematous dermatitis, there must be a clear understanding of allergic eczematous dermatitis, and an understanding of the term eczema itself. The term eczema , which translates as bubbling over, lends itself to confusion and misusage. All too often, the term eczema is used nonspecifically, resulting in confusion for patients and doctors. Although this term is commonly used in other countries, many dermatologists in the United States avoid the term because of its ambiguity but realize the common recognition of the word by the lay public. In general, the unqualified term eczema usually refers to atopic dermatitis. When used in nonatopic settings, eczema is synonymous with dermatitis and requires a qualifying term to be useful (contact dermatitis, stasis dermatitis, or contact eczema, stasis eczema). Throughout this article, dermatitis is used in place of eczema and, with modifiers, refers to all the various eczematous skin eruptions. The term allergic usually refers to an immunologically mediated process in response to an allergen. Allergic contact dermatitis is mediated in part by T-cell activation following exposure to certain antigens contacted by the skin. Urticaria, an allergic disease mediated by IgE antibodies in response to specific antigens, is not considered a dermatitis per se and is not discussed in this article. Atopic dermatitis is frequently considered an allergic dermatitis although the precise immunologic mechanisms in atopic dermatitis are not completely understood. Elevated serum IgE levels plus the coexistence of IgE-mediated diseases seen in atopy (allergic rhinitis and asthma) suggest that atopic dermatitis is triggered by allergic phenomena. This article reviews the pathophysiology, clinical features, and treatment of atopic dermatitis, allergic contact dermatitis, and common dermatitides that have similar presentations but are considered nonallergic (Table 1).

Lymphocyte response to cow's milk proteins in patients with cow's milk allergy: relationship to antigen exposure.

The cellular immune response to cow's milk was measured in patients with challenge-proven cow's milk allergy (CMA), manifested with either gastrointestinal or skin symptoms. After 2-4 weeks on milk elimination, 44 children, mean (SD) age 15.7 (9.4) months, were challenged, and cow's milk-induced lymphocyte transformation was measured before the clinical challenge (Day 1) and/or one week later (Day 8). During the clinical challenge period, 17 (39%) patients showed gastrointestinal reactions, 9 (20%) had urticarial or eczematous skin eruptions, and 18 (41%) were negative to challenge. On Day 1, the mean [95% confidence interval] stimulation index for lymphocytes in patients manifesting CMA with gastrointestinal symptoms, 2.60 [1.60, 4.10], was significantly higher than that in patients with skin symptoms, 1.15 [0.60, 2.30], or patients with negative clinical challenge, 0.83 [0.64, 1.08], F = 9.0, p = 0.001. After the clinical challenge (Day 8), this cow's milk-induced lymphocyte proliferation response was abrogated. At the same time, CMA patients evidenced a significantly higher spontaneous lymphocyte proliferation response in RPMI medium-containing control cultures than those with negative clinical challenge. We conclude that in patients with CMA, the number of circulating cow's milk-sensitized lymphocytes is depleted or their function is impaired after clinical exposure to cow's milk antigens.

Local Immune Response Measured in Blood Lymphocytes Reflects the Clinical Reactivity of Children with Cow's Milk Allergy

Study was made of immune responses in cow's milk allergy by a new immunoassay that measures total Ig-secreting cells and specific antibody-secreting cells during their maturation cycle in peripheral blood. These primed gut-associated lymphoid tissue-derived lymphocytes are assumed to reflect the intestinal immune responses. During diagnostic milk provocation, 15 patients had acute urticarial skin eruptions, eight patients had slow onset of eczema, and 15 showed symptoms from the gastrointestinal tract. A significant increase in IgM-secreting cells (means with 95% confidence intervals) from 382.2 (265, 552) to 621.4 (381, 1013)/10(6) cells, p less than 0.01, but not IgA- and IgG-secreting cells was associated with acute urticaria. In patients with eczematous skin eruptions and gastrointestinal symptoms, the response involved all these Ig isotypes. The magnitude of the postchallenge Ig-secreting cell responses in patients with gastrointestinal symptoms in the IgM class [from 657.9 (428, 1012) to 3544.0 (1696, 7406)/10(6) cells, p less than 0.001] and the IgA class [from 974.6 (590, 1610) to 2482.4 (1528, 4028)/10(6) cells, p = 0.001] significantly exceeded that of the patients with cutaneous symptoms. Notwithstanding the distinct increase in the total number of Ig-secreting cells, the specific antibody-secreting cell response specifically directed against beta-lactoglobulin and alpha-casein was small and inconsistent. These findings indicate that immune exclusion of milk antigens is defective in cow's milk allergy. The quality and extent of the response varied in the three reaction types, suggesting that different immunopathogenic mechanisms are operative in cow's milk allergy.

LOCAL IMMUNE RESPONSE MEASURED BY BLOOD LYMPHOCYTES REFLECTS THE CLINICAL REACTIVITY OF CHILDREN WITH COW'S MILK ALLERGY

To investigate the intestinal immune responses during a diagnostic milk provocation in patients (mean age 13.5 months) with cow's milk allergy (CMA), tola) immunoglobulin-secreting cells (ISCs) and specific antibody-secreting cells (ASCs) from peripheral blood samples were assessed by ELISA plaque assay (ELISPOT). Fifteen patients had acute urticarial skin eruptions, 8 patients had slow onset of eczema, and 15 patients showed symptoms from the gastrointestinal tract A significant increase in IgM secreting cells (geometric means with [95 % confidence intervals]) from 382.2 [265, 552] to 621.4 [381, 1013]/106 cells; t = 2.87, p < 0.01 but not IgA- and IgG-secreting cells was associated with acute urticaria. In patients with eczematous skin eruptions and gastrointestinal symptoms the response involved all these immunoglobulin isotypes. The magnitude of the post-challenge ISC responses in patients with gastrointestinal symptoms in IgM class (from 657.9 [428,1012] to 3544.0 [1696, 7406]/106 cells; t = 4.44, p < 0.001) and IgA class (from 974.6 [590, 1610] to 2482.4 [1528, 4028]/106 cells, t = 3.99. p = 0.001) significantly exceeded that of the patients with cutaneous symptoms. Notwithstanding the distinct increase in the total number of ISCs, the ASC response specifically directed against beta-lactoglobulin and alfa-casein was small and inconsistent. In patients with acute urticaria no antigen-specific response was found, and in patients with eczema and gastrointestinal symptoms it was restricted to IgM isotype. These findings indicate that immune exclusion of antigens is defective in CMA. The quality and extent of the local immune response varied in the three reaction types, suggesting that different immunopathogenic mechanisms are operative in CMA.

Provocative challenge with local anesthetics in patients with a prior history of reaction

Possible allergic sensitivity to local anesthetic agents remains problematic for some patients who could benefit from their use. We retrospectively reviewed all our consultations for evaluation of local anesthetic allergy from 1965 to 1985 to assess the safety and efficacy of skin testing and provocative test dosing with a variety of local anesthetic agents. Fifty-nine patients reported 70 reactions from the administration of six different local anesthetics. Fifty-four patients could name one or more local anesthetic agents they believed were responsible, and five patients named only “caine” drugs. Multiple reactions of the same type to the same agent were considered as one reaction. On the basis of their history of reaction, the patients were categorized as follows: anaphylactoid reactions (urticaria, angioedema, wheezing, or hypotension within 1 to 2 hours of exposure), possible anaphylactoid reactions (tachycardia, dizziness, syncope, breathlessness, or pruritus occurring within 1 to 2 hours of exposure), contact dermatitis (a typical eczematous skin eruption after appropriate cutaneous sensitization), and other reactions (nonanaphylactoid reactions other than those already described or those occurring more than 2 hours after exposure). Fifty-nine patients were administered local anesthetics after skin testing and provocative test dosing, including two patients who required intravenous lidocaine (Xylocaine; Astra Pharmaceutical Products, Inc., Westboro, Mass.) acutely to control cardiac arrhythmias. These two patients had reported anaphylactoid reactions to oral antiarrhythmic drugs of the local anesthetic class. Despite the history of previous reactions, there were no positive skin tests or positive provocative drug challenges in any patients. We conclude that local anesthetics can be safely and effectively used despite the history of previous reactions if skin tests are negative and if incremental challenge is used. Patients reporting immediate reactions to oral and parenteral antiarrhythmic local anesthetics may be skin tested and cautiously challenged with these drugs. A protocol for performing these tests is suggested.