Is recurrent epistaxis from Kiesselbach's area (REKAS) in any relationship to the hemorrhoidal disease?

Vascular diseases are a major threat to human health nowadays. Hypertension, cardiovascular disease and varicose vain disease including hemorrhoids, are now increasingly recognized as inflammatory diseases. The role of inflammation cytokines in the pathogenesis of these diseases is very important. The lamina propria in the nasal mucosa is rich in blood vessels and humoral mediators. Recurrent epistaxis from Kiesselbach's area syndrome (REKAS) was first mentioned as early as 1985. It has been found that 90% of patients suffering from recurrent epistaxis from Kiesselbach area syndrome simultaneously suffered from hemorrhoids. Clinical observations suggest a possible mutual pathophysiologic relationship between Kiesselbach's and anorectal venous plexus. This relationship is also suggested in the reverse direction: significantly more than two thirds of primarily hemorrhoidal patients (83.01%) showed simultaneous vascular dilatations within their Kiesselbach plexuses, but none of these patients had ever have recurrent nose bleeds. There is one more thing they did not have (contrary to REKAS group)--anterior septal deformity. Furthermore, REKAS and hemorrhoidal disease, despite being different clinical entities, frequently appear in the primarily REKAS patients or their closest relatives (more than 90% out of all!). At the same time, all of REKAS patients did have a certain degree of the anterior septal deformity, which primarily hemorrhoidal patients did not have at all. Therefore we presume that Kiesselbach's vascular plexus in the Little's area of the nasal septum belongs to the same group as anorectal venous plexus does (others of this group are brain, esophagus, and lower leg venous system). We also presume that the anterior septal deformity is a crucial factor for the onset of the inflammation of the nasal vestibule skin (vestibulitis nasi), while vestibulitis nasi precipitates the onset of typical recurrent nose bleeds from the Kiesselbach's plexus.

Could we prevent unilateral cleft lip/palate in the future?

Surveillance studies have shown that cleft lip and palate is one of the commonest craniofacial anomalies, occurring in approximately 1 in 500 live births. Previous studies on craniofacial form in unilateral cleft lip/palate subjects have been carried out, but most attention has been focused on the deformity of the bony septum whereas the deformities of the nasal spine and cartilaginous component of the septum had received little attention. Our recent study was based on monitoring a very specific type of nasal septal deformity, type 6, and its relation to the unilateral cleft lip/palate disease. This type is very anteriorly located and refers to the cartilaginous part of the nasal septum and the inter-maxillary bone itself. Rhinoscopic view shows a typical, almost horizontal, unilateral groove at the nasal septum located very anteriorly. At the opposite septal side, but corresponding location, there is so called basal crest. The results of our study showed that the incidence of type 6 septal deformity was very high not only in unilateral cleft lip/palate children (80.6%) but also in their parents (58% in at least one of them). In contrast, in our previous study this type of septal deformity was seen in only 3.7% of non-unilateral cleft lip/palate children before puberty, rising to 7.4% in students and 9.4% in adults. In other words, perhaps we can expect the onset of unilateral cleft lip/palate in the offspring of parents who both have a type 6 septal deformity. Perhaps there is a gene responsible for the onset of both type 6 septal deformity and the cleft. If these clinical entities belong to the same gene, the cleft per se could perhaps disappear from the Earth in a near future owing to the gene therapy which will be able to eliminate it before the baby is born or even conceived.