SLE classification criteria: Is “The causality principle” integrated and operative – and do the molecular and genetical network, on which criteria depend on, support the definition of SLE as “a one disease entity” – A theoretical discussion
AuthorRekvig, Ole Petter
Molecular and cellular aspects of the autoimmune pathophysiology in SLE is linked to the “The causality principle”. SLE Classification Criteria identify per definition disease measures (here: synonymous with classification criteria), but not diagnostic criteria within a classical framework. These two mostly theoretical criteria collections represent a salient conflict between phenomenology and the causality principle – between disease measures and molecular interactions that promote such measures, in other words their cause(s). Essentially, each criterion evolves from immunogenic and inflammatory signals – some are interconnected, some are not. Disparate signals instigated by disparate causes. These may promote clinically heterogenous SLE cohorts with respect to organ affection, autoimmunity, and disease course. There is today no concise measures or arguments that settle whether SLE cohorts evolve from one decisive etiological factor (homogenous cohorts), or if disparate pathobiological factors promote SLE (heterogenous cohorts). Current SLE cohorts are not ideal substrates to serve as study objects if the research aims are to describe etiology, and molecular interactions that cause - and link - primary and secondary pathophysiological events together - events that account for early and progressive SLE. We have to develop SLE criteria allowing us to identify definable categories of SLE in order to describe etiology, pathophysiology and diagnostic criteria of delimitated SLE versions. In this regard, the causality principle is central to define dominant etiologies of individual SLE categories, and subsequent and consequent down-stream diagnostic disease measures. In this sense, we may whether we like it or not identify different SLE categories like “genuine SLE” and “SLE-like non-SLE” syndromes. Many aspects of this problem are thoroughly discussed in this study.