Haemorrhoids are highly vascular cushions of connective tissue in the anal canal, which are normal structures of the human body. Haemorrhoidal disease in clinical practice means that there is an abnormal enlargement of the anal cushions when these transform into “anal nodules”, bleed and/or prolapse. Haemorrhoidal disease is very common. Despite numerous studies undertaken and knowledge accumulated on the aetiology and pathogenesis of haemorrhoidal disease in the last decade, the specific mechanisms responsible for the development of the disease are not thoroughly understood. The pathophysiology is most likely multifactorial and complex, manifested by muscle weakness, intrarectal prolapse, changes in vascular pressure and flow in blood vessels, malformations, sphincter damage and failure, venostasis, inflammatory reactions, endothelin and collagen abnormalities, matrix metalloproteinases activity, etc. Currently, treatment guidelines for the haemorrhoidal disease are based on Goligher’s classification. The classification of haemorrhoidal disease should be submitted to revision by including aetiological factors, the dynamism of prolapse, symptomatology, enteropathogenesis, and gender characteristics. The present review is focused on recent data gained by exploring the anatomy, pathophysiology, classification, theories explaining the development of haemorrhoids, as well as aetiological invasive and surgical treatment modalities.
Infective endocarditis is a disease that affects the endocardium and often alters heart valves, notably the aortic valve. Bacteraemia and valvular endothelial damage play an essential role in the pathogenesis of infective endocarditis. The pertinent literature suggests that neutrophil extracellular traps are important contributors to the development of the disease. However, features of the valvular damage and contribution of neutrophils to the alteration of cardiac tissue are not explored sufficiently. The purpose of this study was to investigate the occurrence and distribution of neutrophilic leukocytes and neutrophil extracellular traps in native aortic valves affected by infective endocarditis, using histopathology and immunohistochemistry assays. In addition, the presence of vegetations on the heart valve was determined. Infiltration of neutrophils into the valvular leaflet was significantly more severe at the free margin (mean 5.89 ± 3.00, p < 0.001) and the middle portion (mean 4.58 ± 3.64, p = 0.032) when compared to the base portion (2.05 ± 1.90). No significant differences in neutrophilic leukocyte infiltrating inflammatory lesions were found between cusp layers. The presence of myeloperoxidase and citrullinated histone expression characteristic of neutrophil extracellular traps was demonstrated by the use of immunohistochemistry in IE-affected valvular leaflets and vegetations. Collectively, the study results suggest that the free cusp margin and its middle portion of the aortic valve are exposed to enforced blood flow; endothelial damage and vegetation formation are likely to occur along with the presence of infective endocarditis-related bacteraemia.
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