Igor

Dear Ladies and Gentlemen, Nonspecific inflammation of lungs (pneumonia) in children is a significant problem in the world. In this regard, World Health Organization intends to spend 39 billions of dollars in 2010-2015 years only to prevent this disease (“New WHO/UNICEF action plan to tackle pneumonia”, November 2, 2009, www.who.com). I’d like to bring your attention to acute pneumonia (AP) with progressive tendency. There appears to be an inability of AP treatment to stop the development of inflammatory process and its complications. Although this patients’ group has been a regular subject of numerous publications, the purpose of this discussion is the search and comparative evaluation of palliative (!), often highly aggressive medical ways of complications but not bases of disease. The impression is formed that intense and serious beginning of AP brings about almost always further development of the lung and pleural complications. Is medical science that has achieved astounding results in many difficult subject (oncology, for example) simply capitulating today in front of ordinary lung’s inflammation? Fundamental reason of negative AP tendency is considered its etiology in modern literature. Moreover, nobody remembers today about “staphylococcal lung’s destruction” which outbreak occurred in 60’s -70’s of last century. During that period complicated forms of AP were caused not only by staphylococcus; however, they were explained by means of spicial aggressive staphylococcal quality. Recently, essential changes have occurred in etiology of complicated forms of AP. Currently, even the most dangerous staphylococcal variety (such as MRSA, for example) is not considered one of the major reasons of AP purulent complications. All accusations are put on streptococcus pneumonia and Haemophilus influenzae (See program of WHO). At the same time, the questions -Why did AP theological changes happen? Why do utterly different bacteria cause very similar changes in pneumonia’s focus? – remain unanswered. And can anybody imagine what AP etiology will be in 30-40 years from now? Unfortunately, we often make use of theoretical explanations that don’t correspond to actual reality. As a rule, we don’t know exactly how and when those explanations were formed and proved; but majority of us would think that the explanation is right simply because it has received common acknowledgment. In this connection, I believe it is important to draw your attention to some facts. These facts are well-known but their essences don’t correspond or even contradict the contemporary AP conception. First of all, the bacterial inflammation is always a conflict between micro- and macroorganisms. In this respect, modern literature about AP mainly examines bacterial side. Part of individual peculiarity of patient’s organism, evolution of patient’s sensibilization and protection, role of ecology and other external factors in these processes is not discussed enough from practical point of view. Secondly, clinical medicine has still to study not only positive outcomes of wide use of antibiotics, but its negative consequences, in particular, etiological dynamics of AP. Thirdly, it is widely known that clinical manifestation of nonspecific inflammation will differ depending on principal disease focus. Pneumonia, tonsillitis or furunculus with identical etiology (by the same microorganism) have their own pathogenesis and individual clinical signs, don’t they? Then why is mechanism of AP development substituted for description of bacterial disease reason? What happens in patient’s organism with AP beginning? What is a distinction between AP pathogenesis and mechanisms of other inflammatory diseases? What is a scheme of AP pathogenesis? To which stage do AP mechanisms have adaptable character and when do vital dangerous changes occur which require compulsory outward help? Where are the answers to other similar questions? Fourthly, pneumonia is not contagious – people get sick with pneumonia. This widespread postulate finds its practical confirmation in absence of strict epidemiological measures in comparison with infections and viral diseases. Pneumonia’s epidemics are not so well known to medical science. Increase of AP cases is observed, as a rule, during the time of influenza and grave viral infections and depends on ecological, climate, and even social factors. Then why is treatment strategy built on “antibiotics alone” as with contagious disease? Furthermore, it is a well known fact that bacteriums-stimulaters of AP can be part of symbiotic microflore, found in healthy people, and be in co-existence with symbiotic marcoorganisms without any troubles. To what degree is it justified to use antibiotics and vaccines in such situations and what consequences will follow such actions? What microorganisms will come instead of depressed ones by this protection? But vacuum cannot exist in biological systems even theoretically, can it? Finally, in modern medical literature we don’t have complete explanation of ineffective treatment in some patients with AP even if treatment was started promptly. Perhaps common principles of treatment don’t correspond to mechanism’s chain of disease?! Why, nevertheless, can AP continue to develop despite active treatment? Why inflammatory process in lung during therapy can not only develop but can also sometimes reach purulent complication without (according to microbiological tests) bacteria in disease’s zone?! The bacterium was liquidated by means of antibiotics but inflammatory process was reached to septic stage – this phenomenon can be found in literature but precise and full explanation is absent. I hope this letter will at least question AP idea and become a basis for serious discussion and following investigation. With best regards, Professor I. Klepikov. P.S.: You can read my point of view regarding this issue based on my own research and clinical trials at http://igorklepikov.blogspot.com/2010/10/acute-pneumonia-in-children-article.html.