Advances which have been made in the field of lipid chemistry and bio chemistry during the last ten years mainly are the results of progress in metho dology. The introduction of isotopic and chromatographic techniques has not only enriched our knowledge of normal lipid metabolism but has also greatly enhanced the understanding of the various lipidoses. This is well illustrated by a comparison of the contents of the present monograph with those of my 1955 review in Handbuch der Inneren Medizin (Springer). In addition to better information about the classic lipid thesaurismoses Nie mann-Pick disease, Gaucher's disease and Tay-Sachs disease, the number of hereditary lipid storage diseases has increased considerably through the recogni tion of new syndromes such as metachromatic leukodystrophy, Fabry's disease, Refsum's disease (heredopathia atactica polyneuritiformis), a-p-lipoproteinemia, and Tangier disease. Conversely, disorders such as Hand-Scholler-Christian disease which has been considered a lipidosis up to 1958 (THANNHAUSER) must now be differentiated from the hereditary disturbances of lipid metabolism. Essential hyperlipemia which at one time seemed to be a well defined entity has now been recognized to consist of a number of subgroups, whose pathogeneses appear to be quite different, and whose classification is by no means definite. Similar problems exist for "essential hypercholesterolemia". Since the knowledge of today is the key for the solutions of tomorrow, we are fortunate that the chapters on lipidoses are supplemented by a comprehensive account of lipid chemistry and biochemistry which has been coordinated by W. STOFFEL.
The presence of monotypism in thick atherosclerotic lesions of black females with G-6-PD mosaicism first reported by the Benditts (1973) has been confirmed in two other laboratories. However, we believe that it is premature to conclude that the finding of monotypism necessarily indicates monoclonal origin of athero sclerotic lesions. We have suggested two alternative explanations for the obser vation of monotypism which we believe must be shown to be invalid before accept ing monoclonal origin as the only plausible way to account for the observed G-6-PD monotypism. One of these two alternatives relates to clonal heterogeneity of cell growth potential, i. e. , during the course of progressive growth of a le sion, progeny of one cell may overgrow all others in a portion of the lesion. The other alternative is that one of the G-6-PD alleles may be linked to genes that afford a preferential survival characteristic in the abnormal environment present in atheroscerotic lesions. Thus, cells with one allele may be able to grow better than cells with the other allele, and this characteristic may be unrelated to "A-ness" or "B-ness". We have studied initiation of lesions in He diet-fed swine and demonstrated that all active lesions that were studied were of multiple cell origin (not monoclo nal). We have studied cell growth patterns in developing atherosclerotic lesions in He diet-fed swine and found evidence consistent with clonal heterogeneity in growth potential of lesion cells.
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