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Lucyna Mastalerz

Publications and source records attributed to Lucyna Mastalerz.

13 recordsLinked to original sources
PubMed2025

Omics in Nonsteroidal Anti-Inflammatory Drugs-Exacerbated Respiratory Disease: Current Evidence From the Upper and Lower Airways.

Nonsteroidal anti-inflammatory drugs (NSAID)-exacerbated respiratory disease (N-ERD) is a mainly type 2 inflammatory condition that combines asthma, nasal polyps, and hypersensitivity to NSAIDs. Its pathogenesis involves both upper and lower airways, yet most studies to date have examined these compartments separately. It remains unclear whether the molecular mechanisms in the nose, sinuses, and lungs are distinct or overlapping-an important gap, given that clinical manifestations of N-ERD involve both sites. In this review, we summarize available omics studies-transcriptomics, proteomics, metabolomics, and epigenomics-performed on upper and lower airways in patients with N-ERD. While omics approaches have revealed new molecular insights, comparisons across studies are limited by heterogeneity in design, controls, and methodology. We emphasize the need for integrated multi-omics analyses and standardized frameworks to better characterize the disease across airways. Such efforts are essential for identifying robust biomarkers and therapeutic targets and for moving toward a systems-level understanding of N-ERD.

Humans↗
PubMed2005

Mechanism of chronic urticaria exacerbation by aspirin.

In some patients with chronic idiopathic urticaria (CIU), aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs) that inhibit cyclooxygenase 1 (COX-1) precipitate wheals and swelling. There is no in vitro diagnostic, and diagnosis can be established only by provocation challenges with aspirin or other NSAIDs. Skin reactions triggered by aspirin are associated with the inhibition of cyclooxygenase, specifically COX-1, but not COX-2, and are characterized by overproduction of cysteinyl leukotrienes (cys-LTs). Aspirin and other NSAIDs should be avoided, but highly specific COX-2 inhibitors, known as coxibs, are well tolerated and can probably be safely used. Evidence has been accumulated that these reactions are due to the interference of aspirin-like drugs with arachidonic-acid metabolism. In this article, we discuss the mechanism of these reactions, and the characteristic course of aspirin-induced urticaria and its management.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed2005

[A case of emphysema suggesting cystic lung disease in computer tomography].

Pulmonary emphysema is anatomically defined as abnormal persistent enlargement of the air spaces distal to the terminal bronchioles, accompanied by destruction of alveolar walls, without evident fibrosis. High-resolution computer tomography (HRCT) imaging is a valuable tool for diagnosis of this disease. The presence of minute cysts distributed evenly through all lung zones is rarely observed in pulmonary emphysema. In such cases, emphysema should be differentiated from other cystic lung diseases. We present a case of a 45-year-old women admitted to our Department with dyspnoea on exertion. Physical examination revealed no abnormalities. A chest radiograph showed diffused interstitial lesions in both lungs; HRCT revealed multiple oval-shaped cysts equally dispersed in all lung areas. The pulmonary function tests revealed increased lung volumes (total lung capacity 114.6% predicted, residual volume 200.6% of predicted), while both vital capacity and FEV1 were decreased (73.6% and 54.0% of predicted volumes, respectively). Diffused lung capacity was normal. Trans-bronchial biopsy was non contributory. Histiological examination of lung tissue obtained by videothoraco-scopy (VTS) was diagnostic for bullous emphysema. The patient had prescribed ipratropium bromide and teophyline. Differential diagnosis, apart from pulmonary emphysema, should take into consideration lymphangioleiomyomatosis, histiocytosis and sarcoidosis.

Diagnosis, Differential↗
PubMed2004

Hypersensitivity to aspirin: common eicosanoid alterations in urticaria and asthma.

BACKGROUND: Aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs) can precipitate adverse reactions in two apparently different clinical conditions: bronchial asthma and chronic idiopathic urticaria (CIU). Recent evidence indicates that the reactions are triggered by the drugs that inhibit cyclooxygenase-1 but not cyclooxygenase-2. OBJECTIVE: To assess whether patients with CIU and aspirin sensitivity share common eicosanoid alterations with patients who have aspirin-sensitive asthma. METHODS: Seventy-four patients with CIU and a history of sensitivity to aspirin and NSAIDs underwent placebo-controlled oral aspirin challenge tests. Concentrations of urinary leukotriene E4 (uLTE4) were measured by ELISA and plasma stable prostaglandin D2 metabolite, 9alpha,11beta prostaglandin F(2) by GC/MS. All measurements were carried out at baseline and after aspirin dosing. Patients were genotyped for the leukotriene C4 synthase (LTC4S) promoter single nucleotide polymorphism. RESULTS: In 30 of 74 patients, the aspirin challenge was positive, resulting in urticaria/angioedema. In these 30 patients, baseline uLTE4 levels were higher than in nonresponders and the healthy control subjects and increased further (significantly) after the onset of clinical reaction. No such increase occurred in subjects with negative aspirin challenge. Baseline uLTE4 levels correlated with severity of skin reactions. Plasma 9alpha,11beta prostaglandin F(2) levels rose significantly in both aspirin responders and nonresponders, although in the latter group the increase occurred later than in the former. In patients who reacted to aspirin, frequency of (-444)C allele of LTC4S was significantly higher than in patients who did not react. CONCLUSIONS: CIU with aspirin sensitivity is characterized by the eicosanoid alterations, which are similar to those present in aspirin-induced asthma.

Adult↗
PubMed2004

Histological spectrum of cutaneous reactions to aspirin in chronic idiopathic urticaria.

BACKGROUND: During a clinical trial, we obtained 16 biopsies of skin eruptions induced by aspirin in patients with chronic idiopathic urticaria (CIU). In this setting, aspirin triggers skin eruptions through a well-established non-immunological mechanism involving the inhibition of cyclooxygenase type I. This presented the rare opportunity to evaluate histological features of a series of skin eruptions induced by a drug acting through a defined mechanism in a controlled experimental setting. OBJECTIVE: Histological analysis of 16 biopsies of skin eruptions induced by oral aspirin challenge in patients with CIU. DESIGN: Microscopic analysis of tissue sections. PATIENTS: 16 patients with CIU. RESULTS: Aspirin (up to 500 mg) induced a restricted range of histological responses with a classic pattern of urticarial tissue reaction occurring in the majority of (12 of 16) cases. Two biopsies showed an interstitial fibrohistiocytic (granuloma annulare-like) reaction pattern. One case showed only a sparse perivascular lymphocytic infiltrate, and paucicellular dermal mucinosis was observed in one case. CONCLUSIONS: Polymorphism of histological patterns induced by aspirin suggests that in addition to the drug-specific mechanisms triggering drug eruptions, individual factors also play a role in determining the ultimate histological phenotype of a drug response.

Adolescent↗
PubMed2003

Safety of cyclooxygenase 2 inhibitors and increased leukotriene synthesis in chronic idiopathic urticaria with sensitivity to nonsteroidal anti-inflammatory drugs.

BACKGROUND: Nonsteroidal anti-inflammatory drugs (NSAIDs) exacerbate various forms of urticaria by a nonallergic mechanism involving inhibition of cyclooxygenases. OBJECTIVES: To assess safety of cyclooxygenase inhibitors in patients with chronic idiopathic urticaria (CIU) and NSAID sensitivity and to evaluate a role of cysteinyl leukotriene metabolism and mast cell activation in sensitivity to NSAIDs in CIU. DESIGN: Aspirin challenge test followed by randomized, prospective, double-blind, placebo-controlled crossover trial with cyclooxygenase 2 inhibitors. SETTING: Tertiary referral center of a university hospital. PATIENTS: Thirty-six patients with CIU. INTERVENTIONS: Aspirin challenge test (up to 500 mg); randomized trial with rofecoxib (up to 37.5 mg) and celecoxib (up to 300 mg) in aspirin-sensitive patients. After completion of the trial, 7 patients received naproxen sodium (500 mg) as a positive control. MAIN OUTCOME MEASURES: Standardized skin examination, skin biopsy with mast cell count, urinary levels of leukotriene E4 (LTE4), and serum levels of mast cell tryptase. RESULTS: Aspirin induced skin eruption in 18 patients. Rofecoxib or celecoxib did not elicit skin eruption in any of the aspirin-sensitive patients. Patients with CIU had higher urinary excretion of LTE4 than healthy control subjects. Basal urinary levels of LTE4 and serum mast cell tryptase were increased in aspirin-sensitive compared with aspirin-tolerant patients. Severity and duration of aspirin-induced urticaria showed a positive correlation with urinary LTE4 excretion. Naproxen precipitated urticaria in 5 of 7 aspirin-sensitive patients and caused further increase in urinary LTE4. CONCLUSIONS: Cyclooxygenase 2 inhibitors do not induce urticaria in patients with CIU sensitive to NSAIDs. Sensitivity to NSAIDs in CIU is associated with overproduction of cysteinyl leukotrienes and mast cell activation and most likely depends on inhibition of cyclooxygenase 1.

Adolescent↗
PubMedDate not supplied

Analgesics and asthma.

The incidence of asthma is increasing throughout the world, which presents both public health and economic concerns. It is widely recognized that in some adult patients with asthma, aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs) that inhibit cyclooxygenase (COX)-1 exacerbate the condition. This is a distinct clinical syndrome called aspirin-induced asthma (AIA). The disease develops according to a characteristic pattern of symptoms. Persistent eosinophilic rhinosinusitis precedes development of nasal polyposis, aspirin hypersensitivity, and asthma. There is no in vitro test, and diagnosis can only be established by provocation tests with aspirin. At the biochemical level, AIA is characterized by a chronic overproduction of cysteinyl leukotrienes. The key enzyme, leukotriene C4 synthase, is overexpressed in bronchi, and its messenger RNA is upregulated in peripheral blood eosinophils. This can be partly related to the genetic polymorphism of the enzyme. The disease runs a protracted course, even if COX-1 inhibitors are avoided. The course of AIA is often severe, and at least half of the patients need systemic corticosteroids to control their asthma. To prevent life-threatening reactions, patients with AIA should avoid aspirin and other analgesics that inhibit COX-1. The incidence of cross-sensitivity to paracetamol in AIA patients is low and, when a reaction does occur, the symptoms experienced are shorter and milder than if the reactions were evoked by an NSAID. Rapidly growing evidence indicates that highly specific COX-2 inhibitors, known as coxibs, are well tolerated and can be safely used by AIA patients.

Anti-Inflammatory Agents, Non-Steroidal↗