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  • Author or Editor: Andres M. Lozano x
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Andrés M. Lozano and Richard Leblanc

✓ The authors report seven individuals from two families, all of whom had aneurysmal subarachnoid hemorrhage. These cases and all reported cases of familial aneurysms (243 aneurysms in 177 patients from 74 families) were submitted to computer-aided multivariate analysis to determine if the aneurysms or the patients who harbor them differ from sporadic aneurysm cases. Familial aneurysms rupture at a smaller size (mean diameter 10.5 mm), and when the patient is younger (mean age 42.3 years and decennial age at peak incidence 40 to 49 years). There is a similar sex distribution (male to female ratio 48:52), a similar incidence of multiple aneurysms (21.5%), and a similar predominance of females over males with multiple aneurysms (2.2:1). Anterior communicating artery aneurysms occur less often in familial cases (19%) than in sporadic cases. In sibling pairs the aneurysms occur at the same or at mirror sites, and rupture within the same decade twice as frequently as randomly selected nonfamilial aneurysm patient pairs. The occurrence of aneurysms at identical and mirror sites is more frequent in familial cases and appears to be a function of the degree of kinship between affected individuals. These observations suggest a genetic basis for the pathogenesis of familial intracranial aneurysms.

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Richard Leblanc, Andrés M. Lozano, Michel van der Rest and Ronald David Guttmann

✓ It has been suggested that a deficiency in the expression of type III collagen may play a role in the pathogenesis of cerebral aneurysms. To test this hypothesis in cases of familial cerebral aneurysms, fibroblast cell cultures were established and the expression of collagen types I and III was studied in a patient with three cerebral aneurysms whose mother and sister also had cerebral aneurysms. Cultured skin fibroblasts were labeled with tritiated proline. The collagens and procollagens were precipitated and run on sodium dodecyl sulfate-polyacrylamide gel electrophoresis after reduction to analyze procollagen chains. Control cell lines were analyzed simultaneously. Quantitation of the ratios of type III to type I procollagen synthesis was achieved by integration of the intensities of the pro-α1 (III), pro-α1(I), and pro-α2(I) bands on fluorograms of electrophoretic gels of medium proteins.

There was no difference in type I and III procollagen levels observed between the cells from the aneurysm patient and those from the control cell lines. These data do not support the hypothesis that familial cerebral aneurysms are caused by a deficiency of type III collagen.