دانلود رایگان مقاله ایمونولوژی تب دوره ای، آفت دهان، فارنژیت و سندرم التهاب گره های لنفی گردنی – سال 2020
مشخصات مقاله:
عنوان فارسی مقاله:
ایمونولوژی تب دوره ای، آفت دهان، فارنژیت و سندرم التهاب گره های لنفی گردنی. لوزه ها چه چیزی را می توانند نشان دهند. مرور نوشته ها
عنوان انگلیسی مقاله:
The immunology of the periodic fever, aphthous stomatitis, pharyngitis and cervical adenitis syndrome; what can the tonsils reveal. A literature review
کلمات کلیدی مقاله:
PFAPA، لوزه ها، تب دوره ای
کلمات کلیدی انگلیسی:
PFAPA – Tonsils – Periodic fever
مناسب برای رشته های دانشگاهی زیر:
پزشکی
مناسب برای گرایش های دانشگاهی زیر:
ایمونولوژی، گوش حلق و بینی
وضعیت مقاله انگلیسی و ترجمه:
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فهرست مطالب:
Abstract
Objectives
Methods
Results
Conclusion
Keywords
1. Introduction
2. Methods
3. Results
3.1. Histological and immunological evaluation of tonsils in PFAPA
3.2. Microbiological evaluation of tonsils
4. Discussion
4.1. Histological and immunological evaluation
4.2. Microbiological evaluation of tonsils
4.3. Limitation of the studies
5. Conclusions
Declaration of competing interest
List of abbreviations
Declarations
Authors’ contributions
Funding
References
قسمتی از مقاله انگلیسی:
1. Introduction
The periodic fever, aphthous stomatitis, pharyngitis and cervical adenitis (PFAPA) syndrome is the most common paediatric periodic fever syndrome [1,2], with a cumulative incidence of 2.2 per 10,000 children up to the age of 5 years in a Nordic population [2]. The hallmarks of the disease are short, regularly occurring episodes of high fever accompanied by at least one of the following major symptoms: pharyngitis, cervical adenitis and aphthous stomatitis [3–5]. Episodes of PFAPA often start during the first few years of life and often spontaneously resolve during late childhood [2,6]. The criteria for establishing a PFAPA diagnosis was suggested by Thomas et al., in 1999 and have been widely used in international studies, however, there is no established international consensus regarding the definition of PFAPA today [7,8]. A dysregulated interleukin (IL)-1 response may play a part in the etiology of the disease [9,10], and PFAPA is currently regarded as an autoinflammatory disease [11]. Unlike the classical hereditary periodic fever syndromes including familial Mediterranean fever, mevalonate kinase deficiency and TNF-receptor associated periodic syndrome, PFAPA has not been defined genetically. Several candidate genes have been proposed as contributing factors to the etiology of PFAPA, and in addition some studies show familiar clustering of the disease. A polygenic basis for the disease is likely, but further studies are needed to elucidate this. As recently reviewed, an environmental trigger causing immunological reactions with febrile flares in a genetically predisposed host seems the best founded model for the disease today [12].
