Chronic anal fissure (CAF) is a painful tear or crack which occurs in the anoderm. The optimal algorithm of therapy for CAF is still debated. Lateral internal sphincterotomy (LIS) is a surgical treatment, considered as the 'gold standard' therapy for CAF. It relieves CAF symptoms with a high rate of healing. Chemical sphincterotomy (CS) with nitrates, calcium blockers or botulinum toxin (BTX) is safe, with the rapid relief of pain, mild side-effects and no risk of surgery or anesthesia, but is a statistically less effective therapy for CAF than LIS. This article considers if aggressive treatment should only be offered to patients who fail pharmacological sphincterotomy. Aspects of anal fissure etiology, epidemiology and pathophysiology are considered with their meaning for further management of CAF. A molecular model of chemical interdependence significant for the chemistry of CAF healing is examined. Its application may influence the development of optimal therapy for CAF. BTX is currently considered the most effective type of CS and discussion in this article scrutinizes this method specifically. Although the effectiveness of BTX vs. LIS has been discussed, the essential focus of the article concerns identifying the best therapy application for anal fissure. Elements are presented which may help us to predict CAF healing. They provide rationale for the expansion of the CAF therapy algorithm. Ethical and economic factors are also considered in brief. As long as the patient is willing to accept the potential risk of fecal incontinence, we have grounds for the 'gold standard' (LIS) as the first-line treatment for CAF. The author concludes that, when the diagnosis of the anal fissure is established, CS should be considered for both ethical and economic reasons. He is convinced that a greater understanding and recognition of benign anal disorders by the GP and a proactive involvement at the point of initial diagnosis would facilitate the consideration of CS at an earlier, more practical stage with improved outcomes for the patient.
Treatment with BT-A is safe. Despite the application of higher doses of BT-A in the treatment of benign anal disorders so far, no severe side effects were observed.
The H. pylori infection in PD patients with motor fluctuations, despite not significantly influencing PK parameters of LD and 3-OMD, may still have important clinical implications.
A chronic anal fissure (CAF) is commonly referred to as an ischemic ulcer. For many years it was thought that sphincteroctomy produces anal sphincter relaxation, enhances microcirculation and promotes CAF healing. The latest studies have shown that fissure healing does not appear to be dependent on reduction in mean resting anal pressure. Our description of the process of CAF healing is based on understanding the balance between nitric oxide (NO) concentration and a level of oxidative and nitroxidative stress in wounds, which is responsible for contraction of smooth muscles (also anal sphincters), endothelial/skeletal muscle cell remodelling and proliferation. Pharmacological sphincterotomy with botulinum toxin (BTX) has an effect on motor endplate but it also has an influence on nitric oxide synthase (NOS) and other agents. Hypoxia in contracted anal sphincters induces vasoconstriction, in part, by decreasing endothelial NOS expression. Clostridium botulinum C3 exoenzyme - Rho-kinase inhibitor reverses this vasoconstriction. CAF is a site where the haemostatic mechanisms are activated. Rho inactivator C3-transferase from Clostridium botulinum abolished thrombin - stimulated endothelial cell contraction. Attenuated biotransformation of Glyceryl trinitrate (GTN) by mitochondrial aldehyde dehydrogenase and suppression of cGMP-dependent protein kinase expression may play a key role in understanding the problem of synergistic action of BTX and GTN. BTX and GTN are different forms of pharmacological sphincterectomies. This mechanism could explain the potentiate effect of BTX action after NO donors application for CAF. The application of BTX releases the blockage in GTN bioactivation in smooth muscle cells and suppresses basal continuous sympathetic activity, causing modulation of anal sphincters. It is responsible for CAF healing.
Symptomatic gastro-esophageal reflux disease (GERD) is a very common disease. The consequence of GERD is not only erosive esophagitis, but also esophageal stricture, Barrett's esophagus and extra-esophageal damage (including the lungs, throat, sinuses, middle ear and teeth). GERD and Barrett's esophagus are also identified as major risk factors for esophageal carcinoma. Therapy with melatonin prevents esophageal injury from acid-pepsin and acid-pepsin-bile exposure in animals, then further studies are required in humans to establish whether a melatonin supplement is able to protect the patients with GERD from erosions, Barrett's and neoplasia.
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