Alergie na bílkoviny kravského mléka (ABKM) je nejčastější alergií kojeneckého věku. Důležitým momentem v její diagnostice je včasné vytipování suspektního pacienta a provedení orálního eliminačně-expozičního testu. S cílem pomoci poskytovatelům zdravotní péče identifikovat rizika alergie vytvořili odborníci skóre symptomů potenciálně souvisejících s alergií na bílkovinu kravského mléka (Cow ́s Milk-related Symptom Score - CoMiSS). Dotazník přináší relevantní přehled o intenzitě symptomů ABKM a napomáhá v hodnocení rizika ABKM u symptomatických pacientů. V roce 2022 byl CoMiSS aktualizován: cut-off se snížil z ≥ 12 na ≥ 10, Bristolská škála stolic byla nahrazena Bruselskou škálou stolic pro kojence a batolata a angiodém byl zařazen jako nový příznak s identickým hodnocením jako kopřivka.
The cow ́s milk protein allergy (CMPA) is the most frequent allergy of infants and toddlers. It is challenging to early recognize the suspected patient and if indicated, start the diagnostic elimination followed by an oral challenge. To help the medical health care provider to identify infant at allergy risk experts published the Cow ́s Milk Related Symptom Score (CoMiSS). The questionnaire brings a relevant overview of CMPA symptoms ́ intensity and helps to work out the CMPA correctly. In 2022 the CoMiSS was updated: the cut-off decreased from ≥ 12 to ≥ 10, the Bristol Stool Scale was substituted by the Brussels Infant and Toddler Stool Scale intended for non-toilet trained subjects, an angioedema was included as a new symptom with equal rating as urticaria.
- Klíčová slova
- Cow ́s Milk-Related Symptom Score,
- MeSH
- alergie na mléko * imunologie metabolismus prevence a kontrola MeSH
- dítě MeSH
- hodnocení rizik metody MeSH
- imunoglobulin E imunologie MeSH
- lidé MeSH
- mléko imunologie MeSH
- Check Tag
- dítě MeSH
- lidé MeSH
- Publikační typ
- přehledy MeSH
Autor rekapituluje mechanismy vzniku FENO v epiteliálních buňkách sliznice dolních dýchacích cest a zaměřuje se na využití tohoto biomarkeru astmatu v klinické praxi i s ohledem na nově nastupující biologickou léčbu těžké formy onemocnění. Frakční vydechovaný oxid dusnatý (FeNO) je endogenní plynná molekula, reflektující neinfekční zánět dýchacích cest. Rozebírá recentní světové práce o významu FENO u omalizumabu, dále u léčby cílené na blokaci interleukinu IL-5, tedy mepolizumabu, reslizumabu nebo receptoru proti IL-5 benralizumabu, které jsou schválené jako přídavná léčba u těžkého refrakterního eozinofilního astmatu dospělých. FENO jako marker astmatu ovlivnitelný biologickou léčbou, a tedy využitelný k hodnocení účinnosti léčby, se však zdá vhodný zejména u dupilumabu (anti‐IL-4 a 13) a nejnověji u tezepelumabu (anti‐TSLP). Biologická léčba zaměřená na IL-5 sice snižuje eozinofilní zánět, ale má omezený vliv na aktivaci epiteliálních buněk, kde se FENO tvoří. Testování FENO je nákladově efektivní a v kombinaci s klinickým hodnocením zlepšuje léčbu astmatu.
Mechanisms of FENO production in epithelial cells in the area lower airways is being resumed. The author focuses on usage of this biomarker in clinical practice and with respect to new established upcoming biological treatment just in severe variants of the disease. Recent publications of FENO are analysed in omalizumab and other types of biological treatment such as mepolizumab and reslizumab, concentrated on IL-5 or receptor for IL-5 benralizumab. They have been approved as an additional treatment of severe refractory eosinophilic adult asthma. FENO as a marker of asthma influenceable by biological treatment can be used to evaluate the efficiency of therapy and it is mainly suitable in dupilumab (anti-IL-4 and 13) and the latest in tezepelumab (anti-TSLP). The biological treatment focused on IL-5 reduces eosinophilic inflammation, however has a limited influence to activate epithelial cells where FENO is being created. The cost to benefit ratio of FENO is advantageous and this biomarker in combination with other clinical assessment improves asthma treatment.
- MeSH
- biologická terapie metody MeSH
- biologické markery analýza krev MeSH
- bronchiální astma diagnóza farmakoterapie MeSH
- eozinofily MeSH
- humanizované monoklonální protilátky aplikace a dávkování farmakologie terapeutické užití MeSH
- imunoglobulin E krev MeSH
- lidé MeSH
- měření vydechovaného oxidu dusnatého * metody MeSH
- Check Tag
- lidé MeSH
Suppressor of cytokine signalling (SOCS) proteins bind to certain cytokine receptors, Janus kinases and signalling molecules to regulate signalling pathways, thus controlling immune and inflammatory responses. Dysregulated expression of various types of SOCS molecules was indicated in multiple types of allergic diseases. SOCS1, SOCS2, SOCS3, SOCS5, and cytokine-inducible SH2 domain protein (CISH) can differentially exert anti-allergic impacts through different mechanisms, such as suppressing Th2 cell development and activation, reducing eosinophilia, decreasing IgE production, repressing production of pro-allergic chemokines, promoting Treg cell differentiation and activation, suppressing Th17 cell differentiation and activation, increasing anti-allergic Th1 responses, inhibiting M2 macrophage polarization, modulating survival and development of mast cells, reducing pro-allergic activity of keratinocytes, and suppressing pulmonary fibrosis. Although some anti-allergic effects were attributed to SOCS3, it can perform pro-allergic impacts through several pathways, such as promoting Th2 cell development and activation, supporting eosinophilia, boosting pro-allergic activity of eosinophils, increasing IgE production, enhancing the expression of the pro-allergic chemokine receptor, reducing Treg cell differentiation, increasing pro-allergic Th9 responses, as well as supporting mucus secretion and collagen deposition. In this review, we discuss the contrasting roles of SOCS proteins in contexts of allergic disorders to provide new insights regarding the pathophysiology of these diseases and possibly explore SOCS proteins as potential therapeutic targets for alleviating allergies.
- MeSH
- alergie * metabolismus MeSH
- antialergika * MeSH
- cytokiny metabolismus MeSH
- eozinofilie * MeSH
- imunoglobulin E metabolismus MeSH
- lidé MeSH
- proteiny SOCS genetika metabolismus MeSH
- Check Tag
- lidé MeSH
- Publikační typ
- časopisecké články MeSH
- přehledy MeSH
Leishmaniasis, a disease caused by parasites of Leishmania spp., endangers more than 1 billion people living in endemic countries and has three clinical forms: cutaneous, mucocutaneous, and visceral. Understanding of individual differences in susceptibility to infection and heterogeneity of its pathology is largely lacking. Different mouse strains show a broad and heterogeneous range of disease manifestations such as skin lesions, splenomegaly, hepatomegaly, and increased serum levels of immunoglobulin E and several cytokines. Genome-wide mapping of these strain differences detected more than 30 quantitative trait loci (QTLs) that control the response to Leishmania major. Some control different combinations of disease manifestations, but the nature of this heterogeneity is not yet clear. In this study, we analyzed the L. major response locus Lmr15 originally mapped in the strain CcS-9 which carries 12.5% of the genome of the resistant strain STS on the genetic background of the susceptible strain BALB/c. For this analysis, we used the advanced intercross line K3FV between the strains BALB/c and STS. We confirmed the previously detected loci Lmr15, Lmr18, Lmr24, and Lmr27 and performed genetic dissection of the effects of Lmr15 on chromosome 11. We prepared the interval-specific recombinant strains 6232HS1 and 6229FUD, carrying two STS-derived segments comprising the peak linkage of Lmr15 whose lengths were 6.32 and 17.4 Mbp, respectively, and analyzed their response to L. major infection. These experiments revealed at least two linked but functionally distinct chromosomal regions controlling IFNγ response and IgE response, respectively, in addition to the control of skin lesions. Bioinformatics and expression analysis identified the potential candidate gene Top3a. This finding further clarifies the genetic organization of factors relevant to understanding the differences in the individual risk of disease.
- MeSH
- cytokiny MeSH
- imunoglobulin E MeSH
- interferon gama genetika MeSH
- kožní nemoci * MeSH
- Leishmania major * genetika MeSH
- myši MeSH
- zvířata MeSH
- Check Tag
- myši MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
BACKGROUND: Pru p 3 and Pru p 7 have been implicated as risk factors for severe peach allergy. This study aimed to establish sensitization patterns to five peach components across Europe and in Japan, to explore their relation to pollen and foods and to predict symptom severity. METHODS: In twelve European (EuroPrevall project) and one Japanese outpatient clinic, a standardized clinical evaluation was conducted in 1231 patients who reported symptoms to peach and/or were sensitized to peach. Specific IgE against Pru p 1, 2, 3, 4 and 7 and against Cup s 7 was measured in 474 of them. Univariable and multivariable Lasso regression was applied to identify combinations of parameters predicting severity. RESULTS: Sensitization to Pru p 3 dominated in Southern Europe but was also quite common in Northern and Central Europe. Sensitization to Pru p 7 was low and variable in the European centers but very dominant in Japan. Severity could be predicted by a model combining age of onset of peach allergy, probable mugwort, Parietaria pollen and latex allergy, and sensitization to Japanese cedar pollen, Pru p 4 and Pru p 7 which resulted in an AUC of 0.73 (95% CI 0.73-0.74). Pru p 3 tended to be a risk factor in South Europe only. CONCLUSIONS: Pru p 7 was confirmed as a significant risk factor for severe peach allergy in Europe and Japan. Combining outcomes from clinical and demographic background with serology resulted in a model that could better predict severity than CRD alone.
BACKGROUND: Idiopathic generalized epilepsy (IGE) is one of the most common epilepsies and is believed to have a strong genetic origin. Patients with IGE present largely heterogeneous neurocognitive profiles and might show some neurocognitive impairments. Furthermore, IGE siblings may demonstrate worse results in neuropsychological tests as well. In our study, we aimed to map the neurocognitive profile both in patients with IGE and the siblings. We also sought to establish a neurocognitive profile for each IGE syndrome. METHODS: The research sample included 110 subjects (IGE n = 46, biological siblings BS n = 16, and healthy controls n = 48) examined. Subjects were neuropsychologically examined in domains of intelligence, attention, memory, executive, and motor functions. The data obtained from the examination were statistically processed to determine whether and how IGE patients (including distinct syndromes) and the siblings differed neurocognitively from healthy controls (adjusted z-scores by age, education, and gender, and composite z-scores of cognitive domains). Data on anti-seizure medication, including defined daily doses, were obtained and included in the analysis. RESULTS: IGE patients and their biological siblings performed significantly worse in most of the neuropsychological tests than healthy controls. The neurocognitive profile of composite z-scores showed that IGE and biological siblings had equally significantly impaired performance in executive functions. IGE group also demonstrated impaired composite attention and motor function scores. The profile of individual IGE syndromes showed that JAE, JME, and EGTCS had significantly worse performance in composite execution score and motor function score. JAE presented significantly worse performance in intelligence and attention. JME exhibited significantly worse composite score in the attention domain. Anti-seizure medication, depression, and quality of life were unrelated to cognitive performance in IGE group. The level of depression significantly predicted the overall value of quality of life in patients with IGE, while cognitive domains, sociodemographic, and clinical factors were unrelated. CONCLUSION: Our study highlights the importance to consider the neurocognitive profile of IGE patients that can lead to difficulties in their education, acceptance, and management of coping strategies. Cognitive difficulties of IGE siblings could support a hypothesis that these impairments emerge from heritable traits.
- MeSH
- epilepsie generalizovaná * MeSH
- imunoglobulin E MeSH
- kvalita života MeSH
- lidé MeSH
- neuropsychologické testy MeSH
- sourozenci * psychologie MeSH
- Check Tag
- lidé MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- MeSH
- 2S albuminy rostlinné MeSH
- alergeny MeSH
- alergie na arašídy * MeSH
- antigeny rostlinné MeSH
- Arachis * MeSH
- bazofily MeSH
- epitel MeSH
- imunoglobulin E MeSH
- lidé MeSH
- rostlinné proteiny MeSH
- Check Tag
- lidé MeSH
- Publikační typ
- dopisy MeSH
- MeSH
- biologická terapie MeSH
- bronchiální astma * imunologie klasifikace terapie MeSH
- imunoglobulin E imunologie účinky léků MeSH
- interleukin-13 imunologie MeSH
- interleukin-4 imunologie MeSH
- interleukin-5 imunologie MeSH
- lidé MeSH
- monoklonální protilátky * terapeutické užití MeSH
- omalizumab terapeutické užití MeSH
- Check Tag
- lidé MeSH
- Publikační typ
- přehledy MeSH
- MeSH
- alergie na latex imunologie prevence a kontrola MeSH
- alergie * diagnóza epidemiologie etiologie farmakoterapie prevence a kontrola MeSH
- anafylaxe diagnóza etiologie imunologie prevence a kontrola MeSH
- chlorhexidin imunologie MeSH
- gynekologové MeSH
- heparin analogy a deriváty imunologie terapeutické užití MeSH
- imunoglobulin E imunologie metabolismus MeSH
- lidé MeSH
- progesteron imunologie MeSH
- proteiny spermatu imunologie MeSH
- Check Tag
- lidé MeSH
- ženské pohlaví MeSH
- Publikační typ
- kazuistiky MeSH
