Demineralization
Historical document, translated for reference. It reflects medical knowledge of the 1920s–30s and is not medical advice.
Summary
This article discusses the historical theory of demineralization, particularly as proposed by French researchers like Albert Robin, who viewed it as a key pathological feature of tuberculosis. It details the methods used to measure mineral loss in urine and tissues, while noting that later research has largely invalidated the theory as a primary cause of the disease.
Encyclopedia article (1928–1936)
DEMINERALIZATION, i.e., the depletion of the organism of inorganic salts, according to the teachings of French authors (Robin, Ferrier), is a characteristic feature of the pathological metabolism of tuberculous patients, as well as "pre-tuberculous" patients, and causes the progression of the process; "remineralization" therapy is based on this doctrine (demineralization in the narrow sense of the word). As early as 1869, Boyer attributed great importance to the decalcification of lung tissue in tuberculosis and recommended calcium salts for tuberculosis. Senator found excessive calcium excretion in tuberculosis. Albert Robin, who distinguished between general and local demineralization, paid particular attention to this issue starting in 1895. Robin judged the demineralization of the organism primarily by the increase in the "demineralization coefficient," i.e., by the increase in the ratio of the inorganic part of the dry residue of daily urine to the total dry residue; in normal conditions, the demineralization coefficient is 30–32%, rising in the first stage of tuberculosis to 36.7, in the second stage to 33.2 (in "pre-tuberculosis" to 31.5, and in the third stage to 29.5). By subtracting chlorine as an element derived primarily from the body's fluids from the total mineral residue, Robin obtained the "coefficient of protoplasm demineralization." Regarding individual inorganic salts, some researchers (in particular Robin and Bournigault) found an increased amount of calcium and magnesium in the urine of tuberculous patients, while others (Dubar-Voisenet) found excessive magnesium excretion in acute, severe tuberculosis. Teissier insisted on the significance of phosphaturia in tuberculosis, especially in acute processes (which, according to Teissier, occurs at the expense of the phosphoric acid of the bones). Robin judged local demineralization on the basis of comparative analyses of the mineral composition of organs. Thus, according to Robin, lung tissue in tuberculosis contains 7.9% mineral salts instead of the 12% norm due to the loss of various salts, including silicic acid, up to 50% of the norm. Healthy areas of lung tissue in the vicinity of tuberculous foci undergo a kind of "chemical hypertrophy" due to phosphoric acid, lime, magnesium, and potassium. Robin found the content of inorganic salts in the bones in pulmonary tuberculosis to be 34.6% instead of the 46.5% norm; hence the known transparency of bones in tuberculosis to X-rays and the frequency of dental caries. Robin also found a reduced salt content in the blood (in 2 cases). Demineralization is transmitted hereditarily to the descendants of tuberculous patients. In the latter, Gaube found increased excretion of calcium and magnesium in the urine. Proponents of the demineralization theory are inclined to attach great biological significance to these observations in matters of immunity and chemotherapy for tuberculosis. Precise studies by later authors, taking into account the entire mineral balance of tuberculous patients, have not confirmed Robin's theory, and it must be recognized as insufficiently substantiated. The pathogenetic factors of demineralization put forward by its adherents are partly non-specific and partly hypothetical, and remineralization therapy for tuberculosis, built on such shaky foundations, cannot become generally accepted. However, individual details of the latter (combating dietary acidosis, etc.) deserve greater attention. Isolated works of recent years confirm disturbances in the metabolism of silicic acid in tuberculosis (Kahle, Dubard). Demineralization in a broader sense, as a negative mineral balance unrelated to tuberculous intoxication, often occurs in states of malnutrition (e.g., osteoporosis of the starving), in intestinal diseases, etc. To explain the pathogenesis of osteomalacia, rickets, and tetany, one cannot accept a primary disturbance of electrolyte metabolism (it is incorrect to interpret similar disturbances of mineral metabolism as "calciprivic constitution" or "calcareous diabetes"); one must take into account the complex dependence of endocrine-vegetative, vitamin, and acid-base balance factors, and finally, the significance of local lesions of bone tissue.
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“Demineralization.” Soviet Medical Encyclopedia. English translation of Bolshaya Meditsinskaya Entsiklopediya, 1st ed. (Moscow, 1928–1936), ed. N. A. Semashko. https://sovietmedicalencyclopedia.pages.dev/article/demineralization/