To save content items to your account,
please confirm that you agree to abide by our usage policies.
If this is the first time you use this feature, you will be asked to authorise Cambridge Core to connect with your account.
Find out more about saving content to .
To save content items to your Kindle, first ensure no-reply@cambridge-org.demo.remotlog.com
is added to your Approved Personal Document E-mail List under your Personal Document Settings
on the Manage Your Content and Devices page of your Amazon account. Then enter the ‘name’ part
of your Kindle email address below.
Find out more about saving to your Kindle.
Note you can select to save to either the @free.kindle.com or @kindle.com variations.
‘@free.kindle.com’ emails are free but can only be saved to your device when it is connected to wi-fi.
‘@kindle.com’ emails can be delivered even when you are not connected to wi-fi, but note that service fees apply.
The present review aims at an insight into the pathophysiology of chronic rhinosinusitis with nasal polyposis through the combination of three tissue sources: (1) nasal polyp, (2) neighboring non-polypoid mucosa (MS) and (3) healthy controls.
Methods
The primary outcomes included three lists of molecules (1) those significantly different between nasal polyp, neighboring non-polypoid mucosa and controls (2) those up/downregulated in nasal polyp, but comparable between MS and controls and (3) those comparable between nasal polyp and neighboring non-polypoid mucosa, but different between NP and controls.
Results
Ten studies investigating a large variety of 68 molecules presented comparisons between nasal polyp and neighboring non-polypoid mucosa in endotype-specified populations. Comparisons between nasal polyp and neighboring non-polypoid mucosa are approached separately for eosinophilic/non-eosinophilic chronic rhinosinusitis with nasal polyposis . The small number of studies prohibits a meta-analysis.
Conclusion
Inclusion of neighboring non-polypoid mucosa in future studies may provide a bias-free list of the molecules that contribute to the actual pathogenesis and preservation of nasal polyps within the chronic rhinosinusitis inflammatory environment.
A wide variety of insults including infectious agents, medications and endogenous and environmental chemical substances may cause injury to the gastric mucosa. This may take the form of inflammation (gastritis), reactive changes without inflammation (termed gastropathy by some authors), or a combination of the two. The histological appearances may be a ‘pattern’ of injury that is non-specific and can be seen in association with several aetiologies, or there may be histological features that are highly characteristic of a single injurious agent. In this chapter, ‘gastritis’ is considered in three sections – patterns of injury (with many potential causes), specific types of gastritis, and gastric mucosal injury related to medical therapies. A practical approach to diagnosis including potential diagnostic pitfalls is emphasised, as is the need for accurate endoscopic and clinical information when interpreting these specimens. Common entities, such as Helicobacter pylori gastritis and reactive gastritis, as well as rare conditions and other infections are considered. The discussion focuses on endoscopic biopsies (the most common specimen seen in practice) but these changes may be present in the resected stomach in the setting of both benign and malignant disease and also, increasingly, in specimens removed at the time of bariatric surgery.
This chapter deals with inflammatory disease affecting the heart, both disease confined to the heart and inflammatory disease where the heart is affected as one among many other tissues. Myocarditis and its classification and investigation are detailed. Rarer forms including eosinophilic disease and giant cell myocarditis are also included. Endocarditis, both infective and non-infective, is discussed. Systemic inflammatory disease such as lupus, systemic sclerosis, rheumatic disease and sarcoid are also illustrated. Aortic inflammatory disease including Takayasu disease is described.
After a general introduction, the classification systems for cardiomyopathy are discussed. The main clinical types are discussed together with their variants. Hypertrophic, dilated, restrictive, non-compaction, mitochondrial and arrhythmogenic cardiomyopathy are all detailed and illustrated. Tables list the many genes associated with development of these cardiomyopathies. Rarer forms such as histiocytoid cardiomyopathy and mitogenic cardiomyopathy are also illustrated.
Eosinophilic angiocentric fibrosis (EAF) is a rare inflammatory fibrosing condition of unknown aetiology that involves the nose or larynx producing mucosal thickening and severe obstructive symptoms. We report the first case affecting a male. He presented with nasal obstruction requiring septoplasty. The clinical and histopathological features of the condition are discussed and a comparison is made with the seven previous reported cases.
Recommend this
Email your librarian or administrator to recommend adding this to your organisation's collection.