In the treatment of atopic dermatitis ultraviolet therapy is considered the second line of treatment, when adverse reactions occur and control is difficult with topical steroid treatment given as first-line treatment. Recently, ultraviolet A-1 (UVA1, 340—400 nm) therapy and narrow-band UVB (311 nm) therapy have been developed and applied to treatment of refractory skin diseases. In Europe, narrow-band UVB therapy is already used more often than psoralens plus ultraviolet A (PUVA) therapy for atopic dermatitis, psoriasis and several other skin diseases. Another newly developed device that has improved and expanded the spectrum of skin diseases amenable to phototherapy is UVA1. With this modality, doses of UVA1 (340 to 400 nm) up to 130 J/cm² are delivered to diseased skin. UVA1 was first used to treat patients with atopic dermatitis, but it has since been found to be efficacious in several other skin diseases, such as localized scleroderma, where other therapeutic options are limited. These two newly developed phototherapies demonstrate that the introduction of new spectra into dermatologic phototherapy has broadened and improved phototherapy as it relates to established indications such as atopic dermatitis.

抄録全体を表示

Recently, in the field of asthma, there has been a substantial number of clinical trials which include health-related quality of life (HRQoL) as one of the outcomes. These studies employ two types of instruments for assessing HRQoL, generic and disease-specific instruments each being used individually or in combination.
It has been proposed that treatments for patients aimed at increasing longevity, prevention of future morbidity, or making patients feel better. To achieve the last purpose, it is considered that HRQoL should be evaluated. Moreover, there are several reports demonstrating only weak to moderate correlations between physiological variables and HRQoL in patients with asthma. This is another reason for the importance of direct evaluation of HRQoL in conjunction with the conventional clinical indices.
Pharmacological interventions based on guidelines seem to improve not only pulmonary function but also HRQoL in patients with asthma. However, all managements do not necessarily improve HRQoL, therefore assessing HRQoL is strongly recommended in clinical trials.
However, the benefit of including HRQoL in evaluation of patients management is still unknown. It is valid that evaluation of HRQoL in clinical practice can both reveal patients problems that were not spontaneously identified by patients themselves and allow physicians focus on specific problems. Until such data are available, the benefit of assessing HRQoL in clinical practice will remain uncertain.
Although conducting more clinical trials that prove efficacy in clinical practice is required, consideration of HRQoL in patients has recently been recognized as an important topic in the asthma field. It can be said that outcomes in health care for asthma will shift from the physiological aspect to humanistic aspect.

抄録全体を表示

The cysteinyl leukotrienes (CysLTs), leukotriene C₄(LTC₄), leukotriene D₄(LTD₄ ) and leukotriene E₄(LTE₄ ) are released in response to specific allergen in nasal secretions from patients with active allergic rhinitis. The symptoms and inflammation of allergic rhinitis can be induced by inhalation of CysLTs. Inflammatory cells from patients with allergic rhinitis express both the synthetic and signaling proteins for the CysLT pathway. CysLTs activate cell migration, in particular eosinophils, endothelial or epithelial cell adhesion and release of cytokines and other oxidative inflammatory mediators. Cytokines may also activate the release of CysLTs from eosinophils and other myeloid cells and also enhance the expression of the CysLT₁ receptor creating an inflammatory amplification cycle. Systemic CysLT₁ receptor antagonists can reduce the inflammation and symptoms of both allergic rhinitis and asthma.

抄録全体を表示

It is now evident that biological agents targeting on the tumor necrosis factor (TNF) have not only induce a substantial clinical response, but also inhibit the structural damage in patients with Rheumatoid Arthritis (RA). Upon the great success of anti-TNF biologicals as the therapeutic modalities of choice in the treatment of inflammatory disorders of unknown etiology, the details of TNF, and anti-TNF biological agents are extensively reviewed, particularly, focusing on those used against RA. So far, nearly one million patients are expected to expose to these agents worldwide. In Japan, chimeric monoclonal antibody to TNFα, infliximab has been approved for Crohn's disease in 2002, RA in 2003, and TNF receptor 2-IgG Fc fusion protein, etanercept had just approved for RA in 2005. Full human anti-TNFα monoclonal antibody, adalimumab is now under clinical trials. Safety profiles of these agents, based on the exposure to one hundred million patients for up to ten years, are summarized. While the experiences using biological agents in Japan are rather limited, the unique circumstances in Asian countries should been taken into account. In this respect, the issues around the anti-TNF biologicals in Japan are finally discussed.

抄録全体を表示

Inhaled corticosteroid (ICS) therapy is a mainstay of bronchial asthma management. Many clinical studies have indicated that an early start with higher doses of ICS contributes to a better prognosis for asthmatic patients, with improved pulmonary functions, airway hyperresponsiveness and quality of life. The current asthma guidelines suggest that once control is achieved, the dose of ICS should be reduced (stepped down) to the minimal level required to control the disease. The rationale for stepping down the dose includes: 1) minimizing adverse effects, 2) contributing to a precise determination of disease severity and 3) achieving better compliance with the therapeutic regimen. However, a one-time reduction in the ICS dose of over 50% results in a high exacerbation rate (50—78%), and predictive markers for the step-down have not yet been established. Leukotriene receptor antagonist (LTRA) or inhaled long acting β₂-stimulant (LABA) have led to successful step-down among patients who require a high dose of ICS to control their condition. When asthma becomes less controllable and thus requires a step-up of therapy, adding LTRA, LABA or theophylline (still a good choice in terms of cost effectiveness) results in better control than doubling the dose of ICS. However, stepwise management is mainly applied to patients with mild to moderate asthma. Severe asthma pathophysiologically differs from mild to moderate asthma and problems in applying stepwise management remain unresolved. Thus, efforts must be targeted towards developing more effective therapeutic strategies with which to manage all types of asthma.

抄録全体を表示

Recent advances in basic and clinical researches of nonsteroidal anti-inflammatory drugs (NSAIDs) are reviewed. Concerning arachidonic acid cascade, recent studies revealed that not only cyclooxygenase (COX) but also terminal enzymes such as prostaglandin E synthase are very important in the understanding of the pathogenesis of inflammation and mechanisms of action of NSAIDs. We also found that some conventional NSAIDs and a selective COX-2 inhibitor exert pro-apoptotic effect on synovial fibroblasts and several cancer cells by COX-independent mechanisms. Clinical indications for use of NSAIDs are broad and include the following: rheumatic diseases; painful and/or febrile conditions; and prevention from thrombotic diseases such as myocardial infarction. In addition, recently developed selective COX-2 inhibitors have been found to be nearly as effective for the same conditions as conventional NSAIDs except with regard to the prevention of thrombosis. The incidence of severe gastrointestinal events in patients treated with selective COX-2 inhibitors has been proven to be lower than patients treated with conventional NSAIDs. However, there was no difference in renal complications between the two groups. Instead, an increased incidence of myocardial infarction after administration of selective COX-2 inhibitors may occur in patients with risk factors for atherosclerotic or thrombotic complications. Further basic and clinical studies remain to be investigated in the future.

抄録全体を表示

The Japanese Pediatric Asthma Guideline was revised in November of 2002. The guideline, the JPGL2002, has several characteristics different from other asthma guidelines. One of the important differences is the classification of asthma severity;the frequencies of asthma symptoms in Steps 2, 3 and 4 of the JPGL2002 are similar to those of Steps 1, 2 and 3, respectively, of the Global Initiative for Asthma (GINA). In the JPGL2002, infantile asthma is classified separately, considering the necessity of special concern due to the characteristic features, and three different protocols for long-term management are provided according to the patients' ages: younger than 2 years, 2 to 5 years, and older than 5 years. For patients older than 5 years, inhaled glucocorticosteroid (ICS) is recommended for asthma with symptoms more than once a month but less than once a week (Step 2). The GINA classifies this as Step 1 and does not recommend the use of ICS. The recommended dosages of ICS for Steps 3 and 4 of the JPGL2002 are, however, smaller than those for Steps 2 and 3, respectively, of the GINA. It should be clarified in future studies whether or not such a use of ICS can lead to earlier and more frequent remission of asthma, hopefully resulting in the asthma being outgrown.

抄録全体を表示

Analysis of data on asthma deaths from the vital statistics throughout Japan and deaths from asthma attacks in six prefectures of Tohoku district provided information on recent trends and insight into possible future issues about asthma deaths in Japan. The vital statistics throughout Japan show a favorable downward trend in the number of asthma deaths in Japan since 1997. In particular, the asthma mortality rate among persons aged 5 to 34 years was less than 0.3 per 100,000 in 2001. In addition, the number of deaths from asthma attacks decreased more rapidly in the Tohoku district and the rate of reduction was correlated with an increase in the sales of inhaled corticosteroids and anti-leukotrienes but not in the sales of inhaled short-acting β-agonists. Moreover, in the 5 year period from 1997 through 2001 it was clear that the number of asthma deaths in persons 75 years and older and those 60 years and older accounted for 61—66% and 86—88%, respectively, of the deaths in persons of all ages. Therefore, the most important future issue about asthma deaths in Japan should be to focus efforts on decreasing the number of asthma deaths in older persons.

抄録全体を表示

Interleukin (IL)-13 is a Th-2 cytokine, known to be involved in allergic diseases. Although IL-13 and another Th-2 cytokine, IL-4, share receptors and signal pathways, having similar biological properties, the critical role of IL-13 alone in vivo in the pathogenesis of bronchial asthma has recently been recognized, based mainly on analyses of mouse models. IL-13 and its signal pathway are thought to be promising targets to develop a therapeutic agent for bronchial asthma. In this article, we summarize the signal transduction pathway of IL-13, the pathological roles of IL-13 in bronchial asthma, and possible therapeutic strategies to block the IL-13 signal.

抄録全体を表示

In the past decade it has become clear that asthmatic patients who are clinically unresponsive, or ”resistant” to glucocorticoid therapy may have T cells which manifest resistance to glucocorticoid inhibition. This is shown by failure of glucocorticoid not only to repress the production of pro-inflammatory, asthma-relevant cytokines such as IL-5, but also to induce the production of anti-inflammatory cytokines, such as IL-10. Molecular mechanisms underlying this resistance are beginning to be defined, and include inappropriate production of transcriptional regulatory proteins (which may bind to and inactivate the glucocorticoid receptor), cytokine-induced modifications of the glucocorticoid receptor (such as phosphorylation), which alter its capacity to bind to ligand, and complex interactions which regulate histone acetylation status and the quaternary structure of DNA itself. Continued study of these phenomena will lead to a better understanding of the ”normal" physiological mechanisms of glucocorticoid action, and may point to new, alternative avenues of therapy for glucocorticoid resistant asthmatics who suffer from severe disease, and for whom as yet no adequate therapy is available.

抄録全体を表示

β-adrenergic agonists have been traditionally classified as strong or weak. Attempts to express their effectiveness in quantitative terms has led to the concepts of potency, which designates the concentration range over which the agonist becomes effective, and the intrinsic activity, which designates the maximal effect produced by agonist at saturating concentrations. In the present review we describe developments in which the molecular effects of the common β-adrenergic agonists on their cognate receptors can be related to their effectiveness. This approach is based on the activation/inactivation cycle of G proteins. It has been formalized so that the effectiveness (that is the efficacy) of each individual β-adrenergic agonist can be expressed as a single numerical value. The agonists may, therefore, be listed is order of efficacy. For the β-adrenergic agonists for which there is accurate data the order is: epinephrine > fenoterol≈procaterol > albuterol≈zinterol≈terbutaline > dobutamine > tulobuterol > ephedrine. The formal model of β-adrenergic agonism also allows a novel approach to the question of agonist specificity and a more rational appraisal of which drugs might be most useful for particular purposes.

抄録全体を表示

Allergy has now become amongst the commonest disease in the world and the patients are increasing. There have been significant improvements in our understanding of allergic disease and its management. However there are still many unclear points in the precise mechanism of allergic diseases and therapy. Recent wide and extensive investigations suggest that the underlying mechanism of allergic disease is closely related to the allergic inflammation. The aim of this review is to offer a state-of-the-art description in our research concerning the allergic inflammation from the immunopharmacological standpoint.

抄録全体を表示

Despite advances and introduction of new and effective anti-asthma therapies, including inhaled corticosteroids and leukotriene modifiers, the mortality and morbidity of asthma is still a worldwide concern. Moreover, asthma is a complex disease (more likely a syndrome) in terms of varied pathogenesis and a marked clinical and pathological heterogeneity. To overcome the clinical limitations in investigating and unraveling this complexity, animal models have been utilized. In many ways, these models have contributed to the clarification of some of the pathogenesis and identified new therapeutic targets for drug development. We have characterized a number of such mouse models of allergic airway inflammation and altered airway function, defining the role of various cells and factors such as mast cells, interleukin (IL)-13 and CD8+ T cells in the development of airway hyperresponsiveness (AHR) and allergic airway inflammation. In these models we demonstrated that mast cells play a role in the development of AHR through stimulation of immunoglobulin receptors (FcRs). Histamine, a potent chemical mediator secreted by mast cells, was shown to contribute to the development of AHR and airway allergic inflammation. In addition, IL-13 was shown to play a critical role in these allergic responses in the lung. To date, CD8+ T cells have not been recognized as much as CD4+ T cells in the pathogenesis of allergic disorders. However, we have recently shown that CD8+ T cells, particularly allergen-primed CD8+ T cells, were potent inducers of IL-13, AHR and allergic airway inflammation. Furthermore, a subset of CD8+ T cells (T effector; T_EFF) was shown to be important in the development of AHR, allergic inflammation and IL-13. Although further investigations are necessary to fully understand the complex interactions between these inflammatory cells, mediators, cytokines and chemokines, these findings provide new insights into the initiation and persistence of asthma and hopefully will lead to new therapeutic strategies for the treatment of asthma.

抄録全体を表示

Background: Differential gene expression in CD3+ T cells from allergic patients stimulated with allergen will provide important information on the responses of T cells.
Methods: After stimulation of peripheral blood mononuclear cells (PBMCs) with mite extracts, levels of gene transcription were examined in CD3+ T cells from allergic patients.
Results: Stimulation of PBMCs from mite specific IgE positive subjects resulted in specific upregulation of MAL transcription levels that was mediated by IL-4 secretion. The MAL protein in IL-4 stimulated primary T cells preferentially localized in glycolipid-enriched membrane (GEM) microdomains. When MAL was exogenously expressed in primary T cells, CD3ζ was concomitantly enriched, along with the expression of MAL, in GEM microdomains.
Conclusions: GEMs are important for the formation and stabilization of TCR signaling complexes. Therefore, MAL may play a role in the formation of GEMs in activated T cells and the high expression of MAL may contribute to Th2 immune response.

抄録全体を表示

Background: Transdermal patches containing tulobuterol, slow-releasing β2-agonist patches, are now widely used in the treatment of asthma in Japan. Unlike inhalational β2-agonists, tulobuterol patches act systemically and may modify the functional status of inflammatory cells in the peripheral circulation. The objective of this study is to examine the effect of tulobuterol on the adhesive interaction between blood eosinophils and endothelial cells.
Methods: Peripheral blood eosinophils and human umbilical vein endothelial cells (HUVEC) were pretreated with either tulobuterol or a control medium, and adhesion of eosinophils to HUVEC was examined using an eosinophil peroxidase assay.
Results: Spontaneous adhesion of eosinophils to resting HUVEC was not modified by tulobuterol. On the other hand, eosinophil adhesion to IL-4 + TNFα-stimulated-HUVEC was inhibited minimally but significantly by tulobuterol. Furthermore, both IL-5- and FMLP-activated adhesions of eosinophils to HUVEC were partially but significantly inhibited by tulobuterol.
Conclusions: Tulobuterol can decrease adhesion of blood eosinophils to endothelial cells. This finding suggests that tulobuterol patches have anti-inflammatory properties, and may therefore contribute to the treatment of airway inflammation in asthma.

抄録全体を表示

Background: Eosinophils and neutrophils take part in the pathogenesis of bronchial asthma. Cellular adhesion through β₂ integrins is crucial for subsequent effector functions in both cell types. We compared α_Mβ₂ expression, cellular adhesion and superoxide anion (O₂^-) release of human eosinophils and neutrophils under uniform conditions.
Methods: Eosinophils and neutrophils from normal volunteers were purified by a magnetic cell-separation system and a one-step gradient method, respectively. Cells were stimulated with platelet-activating factor (PAF) or complement 5a (C5a) on human serum albumin (HSA)-coated surfaces. Expression of α_Mβ₂ was measured by flow cytometry with phycoerythrin-conjugated anti-CD11b monoclonal antibody. O₂^- release was assayed by chemiluminescence using a Cypridina luciferin analogue as the amplifier. Cellular adhesion was assessed by measuring fluorescence intensity of calcein-AM, which was preincorporated in the cell cytoplasm. Cellular morphology was observed with a light microscope.
Results: α_Mβ₂ expression on the neutrophil cell surface was greater than that on eosinophils, both at rest and on stimulation. In contrast, eosinophils exerted significantly greater cellular adhesion and O₂^- release on HSA-coated surfaces than neutrophils. Morphologically, eosinophils showed marked flattening and deformity, while neutrophil shape change was minimal.
Conclusions: Eosinophils and neutrophils showed different activation profiles with stimulation of PAF or C5a on HSA-coated surfaces. In eosinophils the intensity of cellular adhesion and O₂^- release paralleled the upregulation of α_Mβ₂, while in neutrophils the amount of α_Mβ₂ surface expression appeared to be less associated with the degree of cellular adhesion and O₂^- release.

抄録全体を表示

Background: The purpose of present study is to determine the value of serum levels of the soluble form of β₂ integrin-associated glycosylphosphatidylinositol (GPI)-anchored glycoprotein (GPI-80) for monitoring disease activity during the clinical course of the disease, in a total of 24 serum samples from 9 patients with Wegener's granulomatosis (WG).
Methods: The serum soluble form GPI-80 (sGPI-80) concentrations of WG patients were measured by enzyme-linked immunosorbent assay (ELISA). The titers of anti-neutrophil cytoplasmic antibody (ANCA) were assessed by an indirect immunofluorescence method. The serum concentrations of tumor necrosis factor-α (TNF-α), soluble TNF receptor (sTNFR) I and II, soluble interleukin-2 receptor, and soluble intracellular adhesion molecule-1 of WG patients were also measured by ELISA.
Results: The serum sGPI-80 levels were significantly elevated in active WG and were positively correlated with disease activity. At the time of remission, a significant decrease in GPI-80 was observed. The serum sGPI-80 levels were correlated with the ANCA titer and the concentrations of sTNFR I and II.
Conclusions: These findings suggest that sGPI-80 is useful as an additional measure of WG activity.

抄録全体を表示

Background: Influenza virus is a major trigger of asthma exacerbation. Annual vaccination against influenza should be considered for asthmatics. However, the inoculation rates remain low. One reason may be the lack of evidence supporting the benefit of the vaccination for patients with asthma.
Methods: We studied 115 adults with asthma in 2002—2003 and 67 in 2001—2002 and evaluated the effect of influenza vaccination on the prevention of asthma exacerbation during the winter season (December—March).
Results: The rate of asthma exacerbation per person was significantly lower in asthmatics who received influenza vaccination (0.14 ± 0.4) during the 2002—2003 season than in asthmatics who did not (0.35 ± 0.61) (p = 0.037). During 2001—2002 season, the rate of asthma exacerbation in the vaccinated group (0.08 ± 0.41) appeared to be lower than that in the non-vaccinated group (0.27 ± 0.59). However, the difference between the two groups was not statistically significant (p = 0.143), presumably due to the low number of patients receiving vaccination. Severe adverse effects due to vaccination were not observed in the patients analyzed.
Conclusions: Influenza vaccination during the winter season appears to be effective in the prevention of asthma exacerbation and should be recommended for patients with asthma.

抄録全体を表示

Background: Localized mast cell accumulation has been reported in a number of human diseases. Suplatast tosilate has been reported to inhibit IL-3-dependent murine mast cell development, and therefore is expected to suppress mast cell growth proliferation at disease sites. However, there are differences between the growth factors required by human and mouse mast cells.
Methods: Human mast cells were grown in serum-free culture condition from cord blood mononuclear cells with suplatast tosilate. Mast cell number was assessed from the cell numbers counted by a flow cytometer with constant flow rate and Kit+ percentage. Immunochemistry for tryptase was also examined on the cytocentrifuged preparations.
Results: Suplatast tosilate (100 μg/ml ) dramatically inhibited human mast cell development from cord blood progenitors. On the other hand, the growth of 8-wk old mast cells that developed in serum-free media, and which reached over 95% in purity and still maintained proliferation ability, and the growth of the human mast cell line HMC-1 cells were not inhibited by suplatast tosilate.
Conclusions: Suplatast tosilate may be useful for control of human mast cell numbers at the local sites by inhibiting their development from their progenitors.

抄録全体を表示

Background: Salmon roe (SR) anaphylaxis has often been reported and SR-containing foods are designated as 'recommended for allergic labeling'; however, there have been no reports about its allergenicity, including its cross-reactivity. Because its cross-reactivity is controversial, clinicians are often confused concerning education regarding its dietary elimination. The purpose of this study was to examine the cross-reactivity between SR and other kinds of fish roe, salmon, or chicken egg (CE).
Methods: We measured the specific-IgE to SR, herring roe (HR), pollock roe (PR), salmon and CE using RAST in 27 patients with a fish allergy and 26 control subjects. Then, using the sera of 2 patients with SR anaphylaxis, an ELISA inhibition study was performed to examine the cross-reactivity between SR and HR, PR, salmon or CE. We then compared the IgE binding patterns to SR between the anaphylaxis patients and fish allergy patients with immunoblotting.
Results: There were positive correlations between SR and HR or PR, but none between SR and salmon or CE. In the ELISA study using sera from two patients with SR anaphylaxis, IgE-binding to SR was inhibited more than 50% only when the sera were pre-incubated with HR, inhibited almost 50% by PR in a dose-dependent manner, but not inhibited by CE or anisakis. Salmon inhibited the IgE binding to SR more than 50% in a SR-anaphylaxis patient. The IgE binding patterns to SR from anaphylaxis patients were almost identical and unlike those of patients with fish allergy.
Conclusions: There was a cross-reactivity between SR and HR, but no relationship between SR and CE.

抄録全体を表示

Background: Circadian rhythm is a well recognized feature of patients with asthma characterized by a morning dip of the peak flow rate. However, evening dips of asthmatic patients have never been systematically studied.
Methods: We prospectively studied the frequency and clinical characteristics of asthma patients with evening dips. The records of 229 patients for two months were analyzed.
Results: Fifty four patients (23.6%) had repeated evening dips. Comparison of the groups with or without evening dips revealed that the group of patients with evening dips were younger (mean age, 47.3) and had higher asthma steps (mean 2.46) compared to the other group (56.2 and 1.93, respectively). Self-reported causes of evening dips were related to work overload (24.1 %), exercise (9.3%), mental stress (7.4%), allergen exposure (5.5%), cold air (3.7 %), alcohol (3.7%), and unknown (38.8%). Evening dips of peak flow are often related to the daily activity of patients.
Conclusions: Detection of evening dips might be useful to give specific advices to the patients, and be helpful for the prevention and control of asthma exacerbation.

抄録全体を表示

Background: IL-6 is a unique cytokine that has pro- and anti-inflammatory property. The purpose of this study was to clarify the role of IL-6 in the allergic airway inflammation.
Methods: We challenged wild-type and IL-6-deficient mice with ovalbumin (OVA) inhalation after sensitization to OVA.
Results: OVA challenge induced an intrapulmonary eosinophil infiltration and airway hyperresponsiveness in wild-type mice with increased serum IgE levels and enhanced intrapulmonary mRNA expression of T helper type 2 (Th2) cytokines, IL-5 and IL-13. IL-6-deficient mice developed a similar level of airway hyperresponsiveness despite an attenuated eosinophil infiltration and reduced elevation in serum IgE levels after OVA challenge. After OVA challenge, intrapulmonary IL-5 and IL-13 mRNA expression was less evident in IL-6-deficient mice than wild-type mice, while intrapulmonary IFN-γ mRNA expression was more enhanced. Intravenous administration of anti-IL-6 antibodies during sensitization period in wild-type mice caused similar effects as observed in IL-6 deficient mice.
Conclusions: Endogenous IL-6 may have important roles in Th2 polarization in sensitization period accompanied by eosinophil infiltration after acute exposure to aerosolized antigen.

抄録全体を表示

Background: We report a case of Sjögren's syndrome with pulmonary involvement resembling that seen in Wegener's granulomatosis. The patient was a 69-year-old woman who presented with a three-week history of persistent cough and fever. The chest radiograph and CT scans revealed multiple consolidations in the middle and lower lung fields bilaterally.
Methods & Results: Lung biopsy specimens obtained by video-assisted thoracoscopy showed infiltration of the alveoli by lymphocytes with scattered neutrophils, and microscopic vasculitis of the small arteries. The patient tested positive for antineutrophil- cytoplasmic antibodies (ANCA) against myeloperoxidase (MPO-ANCA) and for anti SS-A & SS-B antibodies; however, the test for ANCA against proteinase 3 (PR3-ANCA) was negative.
Conclusions: Based on the presence of the clinical features of the sicca syndrome and positive findings on Schirmer's test and sialoscintigraphy, the patient was given a diagnosis of Sjögren's syndrome with Wegener's granulomatosis-like involvement of the lungs. Neither upper airway nor renal involvement was detected.

抄録全体を表示