DISSEMINATED lupus erythematosus has come to be understood as a "collagen disease" in which there exists widespread systemic alteration of connective tissue. The fundamental lesion is one involving the smaller arteries, wherein degeneration of the subendothelial connective tissue produces homogeneous eosinophilic fibrinoid material. This substance may then extend into the lumen of the blood vessel, inducing thrombosis and consequent infarction of the parenchymal tissue.
A review of the subject* indicates that etiologic concepts of the condition have remained speculative and diverse. For example, Klemperer6 reported recently that histochemical investigation of acute lupus erythematosus disclosed disturbance in metabolism of nucleic acid as one of the pathogenetic factors. On the other hand, Brody7 found that psychologic stress situations seem a consistent factor in the precipitation or exacerbation of the disease.
Central nervous system manifestations, in view of the vascular nature of the disease, are widespread, as may be gathered from
MALAMUD N, SAVER G. NEUROPATHOLOGIC FINDINGS IN DISSEMINATED LUPUS ERYTHEMATOSUS. AMA Arch NeurPsych. 1954;71(6):723–731. doi:10.1001/archneurpsyc.1954.02320420051006
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