bluuebunny/crossref_metadata_2025 huggingface dataset:
A novel mutation in the ATP2C1 gene is associated with Hailey–Hailey disease in a Chinese family
Authors: Liu Zhou Jiang , Yang Tao , Li Xiuchao , Liu Mugen , Wang Qing Kenneth , Liu Jing Yu
Published: December 2008

Background  A three‐generation Chinese family with Hailey–Hailey disease (HHD) was identified and characterized. The proband developed HHD with severe recurrent blisters and crusted erosions involving the body folds. Skin biopsy studies showed epidermal hyperkeratosis and defects in cell‐to‐cell adhesion. Three other members in the family were also affected with HHD and had the same clinical manifestations. The purpose of this study was to identify the pathogenic gene or mutation in the family.

Methods  All exons and exon–intron boundaries of ATP2C1 were polymerase chain reaction (PCR) amplified and sequenced with DNA samples from the proband. Restriction fragment length polymorphism (RFLP) analysis for the intron 23–exon 24 boundary of ATP2C1 was performed in all family members and in 100 normal control subjects.

Results  A novel 2‐bp deletion (c.2251delGT) was detected in exon 24 of the ATP2C1 gene. The mutation was present in the three other affected family members and in two asymptomatic young carriers, but not in the other normal family members or the 100 normal controls. The mutation resulted in a frameshift change and led to the formation of a premature termination codon (PTC) four amino acid residues downstream from the sixth transmembrane domain.

Conclusions  Our results indicate that the novel c.2251delGT (p.V751fs) mutation in the ATP2C1 gene is responsible for HHD in this Chinese family. This study expands the spectrum of ATP2C1 mutations associated with HHD.
Evaluation of treatment with pentamidine for cutaneous leishmaniasis in Suriname
Authors: Van Der Meide Wendy F. , Sabajo Leslie O. A. , Jensema Annigje J. , Peekel Inge , Faber William R. , Schallig Henk D. F. H. , Fat Rudy F. M. Lai A.
Published: December 2008

Background  In Suriname, pentamidine isethionate (PI) is the only drug available for the treatment of cutaneous leishmaniasis (CL). Recently, local dermatologists have observed an increase in CL patients not responding adequately to the standard doses.

Methods  In this study, patient compliance to PI treatment was assessed, and its efficacy was evaluated by comparing the clinical criteria and parasitologic load in week 3 of treatment. Skin biopsies were collected before, during and at the end of therapy and tested by quantitative nucleic acid sequence‐based amplification.

Results  In total, 67 patients with suspected CL were enrolled during the recruitment period, of which only 23 patients with confirmed CL were followed until the end of treatment. All 23 patients were found to be infected with Leishmania (Viannia) guyanensis. A lower cure rate (76–78%) was estimated than that obtained previously (90%), and only 50% of the recruited CL patients finished the complete treatment schedule.

Conclusions  As one‐half of the CL patients were treated insufficiently, a much shorter treatment protocol should be considered to improve the inadequate follow‐up.
Neutrophilic dermatosis of the hands after influenza vaccination
Authors: Wolf Ronni , Barzilai Aviv , Davidovici Batya
Published: December 2008

An otherwise healthy 72‐year‐old man presented with a painful eruption composed of grouped hemorrhagic purulent blisters on erythematous plaques, on both palms of his hands, which appeared 12 h after he had been vaccinated against influenza.

Based on the patient's history, physical examination, histopathological and laboratory findings, the diagnosis of neutrophilic dermatosis of the hands (NDH) was made.

NDH is currently considered a distributional variant of Sweet's syndrome (SS). It is identical to atypical pyoderma gangrenosum (PG) and pustular vasculitis of the hands.

There are only seven reported cases of SS after vaccination, none of them with lesions confined solely to the palms or soles. Our current case is the third one of SS following influenza vaccination.
Rhinomanometry
Authors: Clement P. A. R.
Published: December 2008

The importance of nasal obstruction is stressed as one of the cardinal symptoms in allergic rhinitis and the major symptom of the late phase reaction; therefore the objective measurement of this symptom is of the utmost importance. The international committee on objective assessment of the nasal airway advocated rhinomanometry as a reliable method for measuring tlus symptom. The author's experience with this method after nasal challenge during the early and late phase, in 18 patients and 10 normal volunteers, is discussed. If total nasal resistance is considered then 41% of the patients showed a late phase. When considering unilateral nasal resistance a late phase was observed in 82% of the patients.
Specific nasal provocation test with powder allergen
Authors: Salzano F. A.
Published: December 2008

Reported here are the results of a large‐scale trial conducted under the guidance of Prof Giovanni Motta, which I coordinated. A total of 656 patients with nasal hyperreactivity were recruited in 51 Italian centres (18 in the north of Italy, 20 in central Italy and 13 in the south). The trial's results were as follows. 1) A clear clinical prevalence of sensitization to different allergens in the different areas of Italy, which could be roughly classified thus: a) in Northern Italy birch and grasses were the main species; b) in Central Italy mites prevailed but oleaceae were also sigmficant; c) in Southern Italy panetaria and oleaceae were the prevailing species. 2) Most cases were sensitive to several allergens, although a considerable proportion (22%) actually presented reactions only to one, the main allergen. 3) Taking account of the patients sensitive to only one allergen and those responding to a main allergen, the proportion of patients reacting clinically to only one allergen rises to 64%. 4) The specific nasal provocation test (sNFT) offers specificity comparable. to in vivo diagnostic methods such as the prick test, and in vitro methods such as RAST, but is much more sensitive. 5) The sNPT can be done in any season. 6) The sNPT is highly specific below a threshold value of nasal reactivity, which can be identified for each allergen studied and expressed in Allergenic Units. 7) In patients in whom the prick test shows multiple sensitivity, the specific NPT identifies the allergen presumably responsible for the nasal reactions (main allergen). In the light of these findings double‐blind specific immunotherapy was started, to last 1 year, in 107 patients (49 given placebo and 58 active treatment), with nasal allergy to grasses, parietaria and mites. The results of this treatment were as follows: 74.1% of patients presented a reduction in nasal resistance, measured by dynamic anterior rhinomanometry, indicating relief of nasal obstruction; mucociliary transport time became normal in 81% of patients, meaning that rhinorrhoea had become less marked; there was a significant rise in the nasal reactivity threshold in 74.1% of patients, illustrating the degree of desensitization achieved; nasal IgA increased in 62.5% of patients and IgG in 55.2% indicating improvement in the local immunological picture. No such improvements were detectable in the patients given placebo. In conclusion, therefore, the findings of this trial in allergic rhinitis underline that the specific NPT proved more sensitive than other in vivo and in vitro diagnostic methods and is unquestionably a fundamental investigational approach for assessing nasal allergies, identlfying the allergens causing the symptoms and setting up rational local immunotherapy. The sNPT also showed the efficacy of specific intranasal immunotherapy.
Nasal immunotherapy in pollen‐sensitive children
Authors: Cserháti E. , Mezei G.
Published: December 2008

Subcutaneous specific immunotherapy has a considerable risk of side effects, including severe life‐threatening ones or even death. The disadvantages and problems of this kind of therapy gave rise to looking for new ways of hyposensitization. In allergic rhinitis the local (nasal) immunotherapy may be effective. We studied the efficacy of local nasal immunotherapy (AllerkinR) in grass and ragweed allergic children suffering from seasonal atopic rhinitis. Patients: 36 children (12 with grass pollen, 12 with ragweed pollen immunotherapy, 12 controls). Methods: nasal provocation tests with increasing doses of Allerkin, skin prick test, diary cards. Schedule of the investigations: enrollment of the patients and nasal provocation tests; grass pollen and ragweed pollen preseasonal immunotherapy with increasing doses of Allerkiq during pollen season registration of symptoms and drug consumption; after the season nasal provocation tests. Results: grass immunotherapy: nasal provocation threshold increased (P<0.Ol), symptoms became fewer (P<0.Ol) and drug consumption was less in the active group compared to control. Similar but less expressed tendencies were seen in the ragweed group. After the second year of immunotherapy the need for steroid treatment was significantly (P<0.05) fewer in the immunotherapy group than in the control group. No side effects appeared during the course of immunotherapy, but some patients suffered from mild sneezing or nasal discharge after the Allerkin application. Conclusion: local (nasal) immunotherapy is an effective, safe and not troublesome alternative to systemic immunotherapy.
Milestones in the biology and pharmacology of histamine H1‐receptor antagonists
Authors: Marone Gianni
Published: December 2008

Daniele Bovet's pioneering discovery that a series of compounds possessing anti‐histamine activity reduced the symptoms of anaphylaxis provided the proof that histamine plays a pivotal role as a mediator of allergic reactions. Basophils and mast cells are the major sources of histamine in man and they are thus one of the primary effector cells of allergic inflammation. Some H1‐receptor antagonists posseses a variety of antiinflammatory activity to H1‐‐antagonismin vitroandin vivo. This promising area should be explored further and much remains to be done in the evaluation of the immunodulatory effects of anti‐histamines.
Antihistamines in the treatment of asthma
Authors: Malick Alnoor , Grant J. Andrew
Published: December 2008

Antihistamines were investigated for use in asthma shortly after discovery over fifty years ago. Earlier compounds proved ineffective because of side effects: this class of drugs was not thought useful for asthma, and were actually considered contraindicated. More recent drugs have greater potency, fewer side‐effects, and no evidence of adverse effects in asthma. There are some studies showing second generation antihistamines, especially cetirizine, improve certain parameters of asthma.
Highlights in cardiovascular effects of histamine and HI‐receptor ansgonists
Authors: Genovese A. , Spadaro G.
Published: December 2008

Despite numerous studies, the cardiac actions of histamine are still obscure. Yet, histamine could probably be clinically relevant. It is stored in large amounts in human cardiac tissue, where it is contained in the cytoplasmatic granules of mast cells (1). Mast cells are present in normal human heart tissue; they are more abundant in diseased human heart tissue where they lie in close proximity to blood vessels and between myocytes (2, 3). The histamine content of human heart mast cells is comparable to the histamine content of lung parenchymal and skin mast cells (4). Ultrastructural studies confirmed the presence of mast cells around vessels and between myocytes (2). Consequently, these cells are easily accessible to circulating antigens, drugs and stimuli that activate the cells to release vasoactive mediators which in turn can exert significant cardiovascular effects (5–7).

Histamine possesses arrhythmogenic effects and once locally released, may enhance automaticity and induce triggering activity resulting in severe tachyarrhythmias. The major arrhythmogenic effects of histamine consist in increasing sinus rate and ventricular automaticity, and in slowing atrioventricular conduction (8). In addition, histamine may interfere with depolarization and repolarization through its effects on calcium and potassium currents. These effects are mediated by H2‐receptor (9). Therefore direct activation of histamine receptor can induce cardiac arrhythmias. Consequently, the interference of these histaminergic effects may explain, at least in part, the arrhythmogenic effects described for some second‐generation antihistamines, such as terfenadine and astemizole (10–25).

In this brief review we will discuss the cardiac effects of histamine in experimental animal models and in man, and will review data on the safety of the new second‐generation antihistamines, focusing on their cardiotoxic effects.
Pathophysiology of perennial allergic rhinitis
Authors: Naclerio R. M.
Published: December 2008

Allergic rhinitis involves an early phase, largely mediated through mast cells, and a late phase which involves cellular infiltration and mediator release. In the early phase, mast cells release mediators as a result of antigen cross‐linking adjacent immunoglobulin E molecules bound to mast cell surfaces. This results in an accumulation of histamine which gives rise to the characteristic symptoms of rhinitis ‐ sneezing, itching, rhinorrhoea and congestion. The late phase of the allergic response (hours after challenge) involves infiltration of the nasal epithelium by eosinophils, basophils, monocytes and T‐lymphocytes, which release leukotrienes, kinins, histamine and a host of other mediators. The most important part of the late‐phase response is probably mediated via the production of cytokines (IL‐4, IL‐5, IL‐6, IL‐8, GM‐CSF and RANTES) by mast cells, Th2 lymphocytes or epithelial cells. The infiltration of tissues by cells normally present only in the blood is brought about by the production of adhesion molecules, such as VCAM‐1 and E‐selectin, which cause circulating eosinophils, basophils and T‐lymphocytes to adhere to endothelial cells before moving through the endothelium into the tissue (diapedesis). Neuronal reflexes also play a role in the allergic response, both by mediating local responses to mediators and possibly playing a part in the activation of T‐lymphocytes. The allergic response has also been shown to be less intense in a hot, humid environment, and more marked in a cold, dry environment, possibly due to changes in osmolality of the nasal surface fluid. Similar factors may play a role in the actiology of non‐allergic rhinitis.
Autonomic reflexes and non‐allergic rhinitis
Authors: Jones A.S.
Published: December 2008

Functions traditionally ascribed to the nose include warming, humidification, and filtration of inspired air prior to its passage to the lower respiratory tract. The nose thus conditions inspired air, making it suitable for pulmonary gas exchange. In order to carry out these functions, the nose is subject to a complex series of reflexes mediated via the autonomic nervous system. The effector tissues are the nasal blood vessels and glands. Perennial non‐allergic rhinitis may be divided into two types based on the presence or absence of eosinophilia in nasal secretions. Much circumstantial evidence suggests that non‐eosinophilic non‐allergic rhinitis (NENAR) may be a disease of autonomic imbalance. In a series of studies carried out at the University of Liverpool, patients with perennial non‐allergic rhinitis, and NENAR in particular, were found to have qualitative and quantitative abnormalities in their nasal response to various stimuli as manifested by changes in nasal patency. The nasal response to axillary pressure is much reduced in NENAR patients compared with normal controls, and the normal decrease in nasal resistance in response to standing is abrogated. Isometric exercise has little effect in normal subjects, but those with NENAR demonstrate an increase in nasal resistance. A similar effect is seen in response to the cold pressor test. Of great importance for therapy is the effect of topical fluticasone propionate in patients with NENAR. Treatment normalrzes the damaged nasal reflexes seen in this condition, whereas placebo has no effect. However, abnormalities in other non‐nasal autonomic reflexes (systemic parameters) are not affected by treatment.
The link between the nose and lung, perennial rhinitis and asthma—is it the same disease?
Authors: Rowe‐Jones J. M.
Published: December 2008

Perennial rhinitis and asthma are clinical syndromes representing a range of overlapping pathologies; accurate classification should therefore precede any comparison. Although the sinonasal cavities, trachea and bronchi have a common respiratory mucosa, there are also anatomical differences. For example, the nose has a capacitance vessel network and the lower airways possess smooth muscle, both of which are responsive to neurohumoral influences. The prevalence of rhinitis and asthma has increased over the last three decades. Rhinitis occurs in around 75% of allergic asthmatics while 20% of perennial allergic rhinitics develop asthma. Eosinophils, and their associated proteins and cytokines, may play a central role in both perennial rhinitis and asthma with and without atopy. The characteristic pathology of asthma can be summarized as a chronic, desquamating, eosinophilic bronchitis. Non‐allergic rhinitis with eosinophilia is recognized, but without consistent evidence of epithelial damage. Eosinophils are also present in rhinosinusitis with polyposis, particularly in patients with aspirin sensitivity, in whom asthma also often occurs. Increased mast cell activation and mediator release is evident in both perennial rhinitis and asthma following allergen challenge. The importance of mast cells in non‐atopic asthma and polyposis is also recognized. Adhesion molecules may also be upregulated, with an increased number and activation of Th, lymphocytes. However, allergen‐resultant T‐cell activation may be less marked in the nose than in the lung. Autonomic imbalance also plays a role in both conditions via changes in neural tone to effector tissues, release of neuropeptides, and interplay with cellular recruitment. Pharmacological manipulation of rhinitis and asthma also illustrates the pathological similarities and differences.
Epidemiology of allergic diseases
Authors: SCHÄFER T. , RING J.
Published: December 2008

Schäfer T, Ring J. Epidemiology of allergic diseases.

The escalation of allergic diseases (hay fever, asthma, atopic eczema) over recent decades has been linked to an increase in environmental pollutants. The prevalence of hay fever is associated with genetic predisposition, and some reports show an association with urban areas, socioeconomic status, and combined high allergen and automobile exhaust exposure. In asthma, there is also some evidence for geographical variations in prevalence; exercise challenge tests prove positive more often in urban areas than in rural areas. Although genetic predisposition is the strongest single risk factor for atopic eczema, air pollutants may aggravate the condition by acting as unspecific irritants and immunomodulators, leading to increased immunoglobulin E expression. In a study of 678 pre‐school children, the influence of maternal smoking habits on individual measures of atopy revealed a positive association between smoking during pregnancynactation, and a positive history of atopic eczema. An East‐West German comparative study examining different types and levels of air pollution, i.e. sulphurous (industrial; East) and oxidising (urban; West), showed that the prevalence of atopic eczema was greatest in East Germany. When various direct and indirect parameters of air pollution exposure were measured, the greatest association with atopic eczema was found with NOx exposure (indoor use of gas without a cooker hood), and close proximity to roads with heavy traffic. The increased prevalence of atopic eczema cannot be explained by changes in study methodology over time, or conventional risk factors alone; environmental risk factors may be an important contributing factor.
Epidemiology of pollution‐induced airway disease in Scandinavia and Eastern Europe
Authors: BJÖRKSTÉN B.
Published: December 2008

Björkstén B. Epidemiology of pollution‐induced airway disease in Scandinavia and Eastern Europe.

Several potential environmental factors, particularly air pollutants, have been implicated as causal factors for the increased prevalence of allergic disease in western industrialized countries. However, even when combined, these factors can only partly explain the increase. Differences in prevalence of allergy are apparent between urban and rural areas of industrialized countries, with positive skin prick tests being more common in children living in urban regions. However, the prevalence of atopy is lower in children in central and Eastern Europe, where air pollution poses a major problem, than in Western Europe. Indeed, preliminary data from the International Study of Asthma and Allergy in Children (ISAAC) confirm that the prevalence of childhood atopy is lower in Eastern Europe than in Scandinavia. Although air pollution is undoubtedly associated with the development of allergic disease, other factors connected with western lifestyle, such as changes in diet and living conditions, may play an important role and provide a possible explanation for the higher prevalence of allergic disease in western industrialized countries.
Mechanisms of pollution‐induced airway disease: in vivo studies
Authors: PEDEN D. B.
Published: December 2008

Peden DB. Mechanisms of pollution‐induced airway disease: in vivo studies.

Several studies have investigated the effects of ozone, sulphur dioxide (SO2), and nitrogen dioxide (NO2) on lung function in normal and asthmatic subjects. Decreased lung function has been observed with ozone levels as low as 0.15 ppm ‐ this effect is concentration dependent and is exacerbated by exercise. A number of lines of evidence suggest that the effect on lung function is mediated, at least in part, by neural mechanisms. In both normals and asthmatics, ozone has been shown to induce neutrophilic inflammation, with increased levels of several inflammatory mediators, including prostaglandin E2. However, in normal subjects, none of the markers of inflammation correlate with changes in lung function. The lung function changes in asthmatics may be associated with inflammatory effects; alternatively, ozone may prime the airways for an increased response to subsequently inhaled allergen. Indeed, an influx of both polymorphonucleocytes and eosinophils has been observed in asthmatic patients after ozone exposure. It has been suggested that the effect of ozone on classic allergen‐induced bronchoconstriction may be more significant than any direct effect of this pollutant in asthmatics. SO2 does not appear to affect lung function in normal subjects, but may induce bronchoconstriction in asthmatics. Nasal breathing, whlch is often impaired in asthmatics, reduces the pulmonary effects of SO2, since this water‐soluble gas is absorbed by the nasal mucosa. NO2 may also influence lung function in asthmatics, but further research is warranted. SO2 and NO2 alone do not seem to have a priming effect in asthmatics, but a combination of these two gases has resulted in a heightened sensitivity to subsequently inhaled allergen.
Mechanisms of pollution‐induced airway disease: in vitro itudies in the upper and lower airways
Authors: DEVALIA J. L. , BAYRAM H. , RUSZNAK C. , CALDERÓN M. , SAPSFORD R. J. , ABDELAZIZ M. A. , WANG1 J. , DAVIES R. J.
Published: December 2008

Devalia JL, Bayram H, Rusznak C, Calderón M, Sapsford RJ, Abdelaziz MA, Wang J, Davies RJ. Mechanisms of pollution‐induced airway disease: in vitro studies in the upper and lower airways.

Evidence from both epidemiological and laboratory‐based studies suggests that increased exposure to liquid petroleum and gas‐derived air pollutants [nitrogen dioxide (NO2), ozone, and respirable particulate matter] may play a role in the clinical manifestation of both allergic and non‐allergic airway disease. The mechanisms and cell types involved in pollutant‐mediated effects in the airways, however, are not clear. In vitro studies have suggested that human fibroblasts, B‐lymphocytes, alveolar macrophages, and epithelial cells/cell lines may be involved. Studies of fibroblasts and macrophages have demonstrated that exposure to ozone results in decreased cell viability and increased release of pro‐inflammatory mediators from macrophages. Similarly, studies of B‐lymphocytes have demonstrated that exposure to diesel exhaust particles (DEP) enhances the synthesis of immunoglobulin E by these cells. The airway epithelial cells have received the greatest attention in mechanistic studies of air pollution‐induced airway disease and suggest that these cells are likely to play a pivotal role in the pathogenesis of airways disease. Various studies have demonstrated that exposure of nasal or bronchial epithelial cells to NO2, ozone, and DEP results in significant synthesis and release of pro‐inflammatory mediators, including eicosanoids, cytokines, and adhesion molecules. Additionally, evidence suggests that epithelial cells of atopic individuals release significantly greater amounts of cytokines such as granulocyte‐macrophage colony stimulating factor (GM‐CSF), interleukin‐6 (IL‐6), IL‐8, and regulated on activation, normal T‐cell expressed and secreted (RANTES), on exposure to NO2 and ozone. Studies investigating the biological relevance of epithelial cell‐derived pro‐inflammatory mediators have shown that these enhance eosinophil chemotaxis and eosinophil adherence to endothelial cells, suggesting that pollution‐induced inflammation of the airways is likely to be influenced by modulation of epithelial synthesis and release of these mediators.
Protein modification bv fermentation: effect of fermentation on the potential allergenicity of pea
Authors: Barkholt V. , Jergensen P. B. , Sørensen D. , Bahrenscheer J. , Haikara A. , Lemola E. , Laitila A. , Frøkiær H.
Published: December 2008

The effect of fermentation on components of potential significance for the allergenicity of pea was analyzed. Pea flour was fermented with three lactic acid bacteria, Pediococcus pentosaceus, Lactococcus raffinolactis, and Lactobacillus plantarum, and two fungi, Rhizopus microsporus, var. oligosporus and Geotrichum candidum. Residual antigenicity against antipea antibodies was reduced to 10% by the three lactic acid bacteria and R. microsporus. Reactions to anti‐pea profilin and anti‐Bet v 1 were still detectable after fermentation. The contents of lectin and pea protease inhibitor were not reduced by the microorganisms.
Food‐induced cutaneous adverse reactions
Authors: Wüthrich B.
Published: December 2008

The skin is the most frequently affected target organ in allergy or intolerance of food and food additives. The most common manifestation is acute urticaria (with or without angioedema), accounting for 40–60% of patients with IgE‐mediated food allergy, whereas food additives rather aggravate chronic urticaria (intolerance provocation). The role of food allergy in the pathogenesis of atopic dermatitis is still controversial; however, there is no doubt that, particularly in infants and young children, food allergens can induce atopic dermatitis or aggravate skin lesions. In adults, food allergy as a cause or a trigger of atopic dermatitis is very rare. However, in food‐allergic patients with atopic dermatitis, the ingestion of the food item can provoke the whole spectrum of IgE‐mediated symptoms, from oral allergy syndrome to severe anaphylaxis. Skin symptoms can also be induced not only after food ingestion in sensitized people, but also after direct skin contact, as lipophilic food allergens can penetrate the skin via the hair follicles or when the skin barrier function is defective. Immediate contact reactions of the skin are a heterogeneous group: they include not only contact urticaria (contact urticaria syndrome) on an immunologic or nonimmunologic basis, but also allergic or nonallergic eczematous reactions caused by food proteins (protein contact dermatitis). A prototype is baker's eczema in a restricted sense with immediate‐type sensitization to flour. Atopic eczema provoked by direct contact of the skin with food must also be taken into consideration. Finally, very rarely, allergic contact dermatitis that is due to type IV sensitization to food or food additives (positive delayed type reaction in the patch tests) can occur. The oral ingestion of these foods may provoke in these patients a generalized eczematous rash or dyshidrosiform reactions (vesicles) of the fingers, palms, and soles.
Life cycle and reproduction of house‐dust mites: environmental factors influencing mite populations
Authors: Hart B. J.
Published: December 2008

An understanding of the life cycle of house‐dust mites, as well as environmental factors influencing mite populations, can be exploited in mite control. The most important limiting factor for house‐dust‐mite populations is air humidity. House‐dust mites osmoregulate through the cuticle and therefore require a high ambient air humidity to prevent excessive water loss. In addition, the supracoxal glands actively take up ambient water vapour, and the protonymph stage of the life cycle is resistant to desiccation. Larger house‐dust‐mite populations are found when the absolute indoor air humidity is above 7 g/kg (45% relative humidity at 20°C). Consequently, ventilation by air‐conditioning systems is being developed as a means of control. A number of other aspects of the domestic environment are also being manipulated in an integrated approach to render the habitat less suitable for mites. The potential exists for developing models for house‐dust‐mite populations, environmental characteristics, and the effects of various approaches to control.
Distribution and abundance of dust mites within homes
Authors: Colloff M. J.
Published: December 2008

The distribution and abundance of dust mites can be modelled on three scales: the microhabitat scale (different habitats within homes), the macrohabitat scale (between homes), and the regional scale. This paper focuses on the first. Those parts of a home in which dust mite populations thrive will tend to be homogeneous in respect of key habitat suitability determinants. The more widespread such determinants, the greater the risk of high mite populations and allergen load. Habitat suitability determinants include an adequate textile substratum, optimal temperature and humidity, and food resources of appropriate quality, as well as other, currently unknown, requirements. Each determinant will have a characteristic distribution within any home, and they can be conceptualized as a series of overlays, or three‐dimensional Venn diagrams, with the areas of overlap representing the most suitable sites for mite survival. That a population of dust mites is focused by constraining biotic and abiotic determinants means that spatial and temporal distribution and abundance are predictable, because the characteristics of the principal foci define optimal conditions for population growth. This concept, known as “focality”, provides a framework for prediction of sites of high density of mite population and allergen exposure, as well as a basis for manipulating the microenvironment for control purposes.
Occurrence of mites in Norway and the rest of Scandinavia
Authors: Mehl R.
Published: December 2008

This paper gives a faunistic review of mites that have been recorded in the indoor environment, particularly homes, barns, and stored products, in Norway and the other Scandinavian countries. Some preliminary results are given from unpublished investigations in Norway. Seven species of pyroglyphid mites have been recorded: Dermatophagoides pteronyssinus, D. microceras, D. faunae, D. evansi, Euroglyphus maynei, Gymnoglyphus longior, and Hirstia chelidonis. D. pteronyssinus was the predominant species, followed by D. microceras in Scandinavia and D. farinae in Denmark. D. evansi was detected in poultry houses in Norway. Lepidoglyphus destructor was the predominant species in barn dust, but large populations of Acarus, Tyrophagus, Tydeus, and Tarsonemidae also occurred. In humid homes, Glycyphagus domesticus was found in high numbers. The result of quantification of mites depends on the method for examination of dust. When one proposes limits for the concentration of mites in relation to risk of allergic sensitization and provocation of symptoms, reference should be made to a well‐described method for sampling and analyzing dust. The number of mites should be given per area, not only per weight unit of dust. The number of mites per area indicates the number of mites in the home. The number of mites per weight unit of dust describes the concentration of mites in the vacuum cleaner.
Allergens from mites: implications of cross‐reactivity between invertebrate antigens
Authors: Aalberse R. C.
Published: December 2008

Group 1 and 2 allergens are probably the most important mite allergens. Some mite allergens, such as tropomyosin, are widely cross‐reactive. The prevalence of sensitization to invertebrates cannot be based solely on skin test or serologic data with the allergen extracts currently available. Purified (recombinant) allergens, selected for low cross‐reactivity, are urgently needed.
Mite‐allergen levels in Norwegian homes
Authors: Gaarder P. I.
Published: December 2008

The scarce data published on mite sensitization and mite‐allergen levels in Norway indicate that the mites may not be of the same importance in allergic disease in Norway as in countries such as the UK and the rest of Europe. The problem also involves the low allergen levels and small amounts of dust collected for allergen determination, and when the level is to be expressed as mg/g, the lower detection limit will often vary from sample to sample, giving within the same investigation results such as < 0.2 μg/g, < 0.5 μg/g, and even <2.0 μg/g. The use of allergen levels expressed instead per area (μg/m2) at least results in a uniform lower detection limit, making statistical analysis easier.
Mite allergens: significance of enzymatic activity
Authors: Hewitt C. R. A. , Foster S. , Phillips C. , Horton H. , Jones R. M. , Brown A. P. , Hart B. J. , Pritchard D. I.
Published: December 2008

Ten years ago, the cloning and sequencing of a cDNA encoding the group I allergen of house‐dust mites unequivocally determined that protein allergens may have biochemical functions in addition to their ability to bind IgE. Since this discovery, several groups have speculated that the biochemical activities of allergens, or substances associated with allergens, may be involved in their immunogenicity or allergenicity. This paper will focus on just one biochemical function, proteolytic activity, and will be illustrated by examples of our own work that we believe support the hypothesis that this category of molecules are endowed with the properties of proallergic adjuvants.
Mite allergens. Collection, determination, expression of results, and risk levels for sensitization and symptom induction
Authors: Dreborg S.
Published: December 2008

The presence of mite allergens in dust can be determined by counting mites at different stages of development in dust and by determination of the major allergen content (Der p 1) in dust and air, which is crucially important to allergic patients. For comparison of results, similar methods for collection of dust and air must be used. Due to their size, mite bodies and fecal particles are airborne only directly after disturbance. Special filters should be used for dust collection, and upholstered surfaces should be vacuumed for 2 min/m2 (minimum 4 m2) and hard surfaces for 1 min/m2 (minimum 8 m2). Heavy contaminations should be removed. Preferably, the method given in the ISAAC study should be followed. Samples should be deep‐frozen for at least some days to kill the mites. ELISA techniques, preferably using polyclonal antibodies and antigen with all isoforms present, should be used for determination of allergens. The allergen load has been given in ng/g of dust, but allergen/m2 or per sample area should be preferred. Allergen in the air should be given in pg/m3. A tentative limit of 2000 ng/g was proposed for sensitization and asthma. This limit is still valid on a population basis, but recent data indicate that highly susceptible young children become sensitized at concentrations 10–100 times lower and that ng levels of cat allergen/m3, as found in schools, induce chronic asthma.
Importance of indoor allergens in the induction of allergy and elicitation of
Authors: Custovic A. , Simpson A. , Woodcock A.
Published: December 2008

During the last few decades, many countries have experienced an increase in the prevalence and severity of asthma. Over the same period, the population in the developed world has retreated indoors, and homes have become better insulated and more energy efficient, resulting in a warm and humid environment with low ventilation rates, ideally suited to house‐dust‐mite population growth throughout the year. Increasing exposure and increasing sensitivity to indoor allergens represent a progressively higher risk factor for the development of asthma. The development of sensitivity to indoor allergens and the symptoms and severity of asthma in later childhood are directly related to the exposure to allergens in infancy. It was relatively straightforward to demonstrate a quantitative linear dose‐response relationship between exposure to house‐dust‐mite allergens and subsequent sensitization. However, showing the same for exposure and asthma severity has been more difficult, as the relationship between exposure and asthma symptoms in already sensitized individuals is much more complex than in the case of exposure and sensitization. Nevertheless, sensitized individuals are likely to have more severe asthma if exposed to high allergen levels than if their level of exposure is low. Sensitization to house‐dust mites is a major independent risk factor for asthma in all areas where climate is conducive to mite population growth. The relevance of allergens other that mite is not consistent between different areas, and depends on the climate, habits, and socio‐economic features of the local community. It would appear that presence of mite allergens in homes “overshadows” other allergens (e.g., cat, dog, or cockroach) as a risk factor for sensitization and subsequent development of allergic disease. It is possible that this is the consequence of the difference in inherent potency between allergen sources, and the question of why mite allergens are so potent in inducing sensitization and atopic disease remains to be answered.
The structure of major birch pollen allergens ‐ epitopes, reactivity and cross‐reactivity
Authors: Spangfort Michael D. , Mirza Osman , Holm Jens , Laisen Jørgen N , Henning Løwenstein Henrik Ipsen
Published: December 2008

To cite this article:

Spangfort Michael D., Mirza Osman., Holm Jens., Laisen Jørgen N., Ipsen Henrik., Løwenstein Henning. The structure of major birch pollen allergens ‐ epitopes, reactivity and cross‐reactivity. Allergy 1999, 54, 23–26.

Copyright © Munksgaard 1999 ISSN 0108–1675
Can the natural course of allergy and asthma be changed by allergen vaccinations?
Authors: Valovirta E.
Published: December 2008

To cite this article:

Valoviita E. Can the natural course of allergy and asthma be changed by allergen vaccinations? Allergy 1999, 54, 37–29.

Copyright © Munksgaard 1999 ISSN 0108–1675
Pharmacological modulation of the allergic response: different modes of action
Authors: Scadding G.
Published: December 2008

To cite this article:

Scadding G. Pharmacological modulation of the allergic response: different modes of action. Allergy 1999, 54, 39–42

Copyright © Munksgaard 1999 ISSN 0108–1675
Inhaled corticosteroids versus anti‐leukotrienes: a literature review on the clinical effects
Authors: Ind P.W.
Published: December 2008

To cite this article:

Dr. Ind Philip W. Inhaled corticosteroids versus anti‐leukotrienes: a literature review on the clinical effects. Allergy 1999, 54, 43–46.

Copyright © Munksgaard 1999 ISSN 0108–1675
2. Surgical treatment of nasal polyps: past, present and future
Authors: Stammberger H.
Published: December 2008

Considerable changes have taken place over the last two decades in the surgical approach to nasal polyposis. The advent of the endoscope has enabled earlier detection and less traumatic and more precise surgical treatment of diseases presenting with nasal polyps. The concept of functional endoscopic sinus surgery (FESS) offers individualized surgery according to the respective patient's disease, and routine radical surgical procedures can be avoided with good functional results. In patients with aspirin intolerance, allergic fungal sinusitis and asthma, nasal polyposis is histologically dominated by dense eosinophilic infiltration and requires a more aggressive approach, often involving combined therapy with corticoster‐oids. In these cases, extensive postoperative care and follow‐up is required to preserve the good postoperative result and to prevent regrowth of polyps.
5. Clinical performance of fluticasone propionate nasal drops
Authors: Holmström M.
Published: December 2008

The efficacy and safety of fluticasone propionate (FP) nasal drops were investigated in two multicentre, randomized, placebo‐controlled trials. Patients received FP 400 μg once or twice daily for 12 weeks and then FP 400 μg once daily for a further 12 weeks. FP 400 μg significantly reduced polyp size and improved peak nasal inspiratory flow, rhinitis symptoms and sense of smell when administered twice daily. Significant reductions in polyp size were not achieved with once daily administration, but clinical benefits were observed for peak nasal inspiratory flow. Both dosing regimens were well tolerated, with an overall incidence of adverse events which was similar to placebo.
IL15 gene variants are not associated with asthma and atopy
Authors: Pinto L. A. , Depner M. , Steudemann L. , Klopp N. , Illig T. , Von Mutius E. , Kabesch M.
Published: December 2008

Background:  Interleukin 15 (IL15) promotes activation and proliferation of CD8+ T cells and enhances the differentiation into Th2 cells. A previous study described five polymorphisms in the IL15 gene to be associated with asthma in a haplotype analysis.

Aim:  We selected HapMap tagging single nucleotide polymorphisms (SNPs) from IL15 to systematically investigate these IL15 associations in a large population‐based sample.

Methods:  Genotyping of seven IL15 SNPs was performed using MALDI‐TOF MS in a cross‐sectional study population of 3099 children from Dresden or Munich (age 9–11 years). All children were phenotyped by standardized and validated protocols for atopic phenotypes. Effects of single SNPs and haplotypes were studied using sas 9.1.3 and haploview. Equivalence tests were performed to prove the significance of negative results.

Results:  Neither single IL15 polymorphisms nor haplotype analyses showed associations with asthma or atopy after correction for multiple testing.

Conclusion:  These results do not confirm previous case–control studies and suggest that IL15 gene variants do not play an important role in the development for asthma or other atopic disorders.
Successful ABO‐incompatible heart transplantation in a child despite blood‐group sensitization after ventricular assist device support
Authors: Urschel S. , Dalla Pozza R. , Loeff M. , Schmitz C. , Sodian R. , Schmoeckel M. , Kowalski C. , Netz H.
Published: December 2008

Abstract:  In the first two yr of life blood‐group incompatible (ABO‐incompatible) heart transplantation can be performed leading to immune tolerance to donor blood group. Antibody titers should be below 1:4. VAD use is correlated with sensitization toward blood‐group antigens. A boy was diagnosed with dilated cardiomyopathy at nine months of age and listed for 0‐compatible transplantation. Progressive heart failure required implantation of a left VAD. His listing was extended for ABO‐incompatible transplantation despite antibody titers of 1:32 anti‐A and 1:8 anti‐B. After 26 days on VAD, he was transplanted with a B donor heart. No hyperacute or acute rejection occurred in 12 months post‐transplant. Anti‐B antibodies rose to a maximum of 1:2. No use of rituximab or plasmapheresis was required. There are no signs of graft vasculopathy. This indicates that inclusion criteria for ABO‐incompatible transplantation may be extended to immediate cases. This is the first case with a healthy immune system to show signs of tolerance development after ABO‐incompatible heart transplantation with increased prior antibody titers and without specific treatment.
Hemodynamic effects of vasopressin antagonism and angiotensin I converting enzyme inhibition during halothane anesthesia in sheep
Authors: Ullman J. E. , Hjelmqvist H. , Rundgren M. , Leksell L. G.
Published: December 2008

The hemodynamic effects of separate and combined intravenous administration of the vasopressin (AVP) V1‐receptor antagonist SK&F 100273 (10 μg/kg) and the angiotensin I converting enzyme inhibitor captopril (20 mg+ 1 mg/h) were studied in 12 sheep during stable halothane anesthesia (1.5% end‐tidal conc.). The separate blockade of either V1‐receptors or angiotensin II (ANG II) synthesis induced a small (7–10%), but significant, fall in mean systemic arterial pressure (MSAP), whereas the combined treatment caused a 30% reduction in blood pressure. The changes in systemic vascular resistance paralleled those of the MSAP. Consequently, the cardiac output was largely unaffected by the interference with AVP effects and/or ANG II synthesis. The halothane anesthesia effectively increased the plasma levels of AVP and ANG II, and plasma renin activity without any relation to changes in MSAP. When either the AVP effects or ANG II synthesis were blocked separately, there was a slight tendency for a compensatory increase of the unimpeded hormonal system. It is concluded that halothane anesthesia increases the plasma levels of AVP and ANG II in sheep, and that the maintenance of the arterial pressure is dependent on the concurrent vasopressor effects of the two hormones in this situation.
Acute cardiovascular and central nervous system toxicity of bupivacaine and desbutylbupivacaine in the rat
Authors: Rosenberg P. H. , Heavner J. E.
Published: December 2008

Desbutylbupivacaine, a major metabolite of bupivacaine, is known to accumulate during long‐term continuous infusion blocks in man. Its acute toxicity in comparison with that of bupivacaine has not been studied. In a lightly anaesthetized rat model, bupivacaine (2 mg/kg/min, N = 10) or desbutylbupivacaine (4 mg/kg/min, N = 10) was infused i.v. until asystole. Arterial blood pressure, ECG and EEG were continuously recorded. The mean doses of bupivacaine producing cardiac toxicity, i.e. arrhythmia (12.4 mg/kg) and asystole (24.0 mg/kg), were approximately half of those of desbutylbupivacaine. Seizure activity on the EEG was observed in only one of the desbutylbupivacaine‐infused rats while all rats receiving bupivacaine developed seizures (mean dose 5.2 mg/kg). Desbutylbupivacaine infusion caused a decrease in arterial blood pressure greater than that resulting from bupivacaine infusion. When desbutylbupivacaine 0.67 mg/kg/min was coinfused with bupivacaine 2 mg/kg/min, the cardiovascular toxicity of bupivacaine was clearly potentiated. The EEG parameters were affected in a similar fashion as when bupivacaine alone was infused. In this rat model, desbutylbupivacaine was about half as toxic as bupivacaine judged by cardiac parameters, and clearly less toxic to the central nervous system than bupivacaine.