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      Anonymous
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      H. pylori is a chronic and common infection throughout the world, with a higher prevalence in developing countries. Without a significant animal or environmental reservoir for human strains of H.pylori, person-to-person contact appears to be the most likely mode of transmission. Exactly how the organism is transmitted from the stomach of one person to that of another remains unclear. Traditional risk factors for ulcer disease, such as smoking, aspirin, and alcohol, interact with H. pylori infection are invoked. The long term neoplastic consequences of this infection also must be kept in the mind.

      The features of HP in the stomach and duodenum are well-known. Here I want to focus on certain aspects of this infection which are not usually dealt with while discussing on this subject. And I think it may be of some interest to the general practioners. This infection is implicated in the aetiology of otherwise unexplained iron-deficiency anaemia, idiopathic thrombocytopenic purpura (ITP) and vitamin B12 deficiency. It may be because the stomach plays an important role in the blood formation. The normal gastric juice contains a special substance known as intrinsic factor secreted by gastric mucosa. This intrinsic factor reacts with the extrinsic factor containing in the food to produce a product which is an anti-anaemic substance. This is absorbed from the gut and transported to liver from where bone marrow utilises this substance for the blood formation. From this it can be inferred that any serious affliction of gastric mucosa can interfere with the blood formation. H.pylori infection by virtue of its damaging effect might prevent the absorption of above mentioned factors and predispose to iron deficiency anaemia and ITP. When treating such blood abnormalities, H pylori should be sought and eradicated.

      Apart from this, there are extra gastric disorders caused by H pylori such as cardiovascular and neurological manifestations such as stroke and Parkinson disease. Basic pathology in both strokes and coronary artery disease is the same, that is atherosclerosis of arterial walls. Also inflammation and infections such as H pylori are incriminated in the causation of atherosclerosis. The inflammation active inflammatory process in atherosclerosis pathogenesis of the coronary circulation is growing. Significantly, monocytes and macrophages are recognized as components of atheromatous plaques for several years. For this reason, chronic inflammation is considered as a risk factor for CHD, and vascular injury, inflammation, and thrombosis are considered to cause atherosclerosis.

      The following table which has come in ‘World Journal of Cardiology’ Jan 2015 gives an idea regarding the above mentioned association between H pylori and coronary artery disease:

      http://www.ncbi.nlm.nih.gov/pmc/article … /table/T1/

      In this context it may be pointed out that when we encounter gastric bleeding with the use of aspirin in coronary artery disease, H pylori should be looked into and when treated the bleeding would be less alarming subsequently. In H pylori-positive patients eradication treatment improves the bioavailability of thyroxine and l-dopa.

      UA Mohammed

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