ACTA ENDOCRINOLOGICA (BUC)

The pathogenesis of type 1 diabetes became a history longer and longer. There are 40 years since the immunogenetic theory of type 1 diabetes has been launched. Near this anniversary a challenge of this theory was recently published. We give here our interpretation of primary cause of type 1 diabetes which must be connected with the pathogenesis of other phenotypes of diabetes which has a main similar mechanism: the β-cell dysfunction.

In the past years a high interest has been observed for understanding the early stages of type 1 diabetes. That interest has been stimulated by the failures of the various “preventive” approaches of the autoimmune mechanism operating in this phenotype, carried out in young diabetic patients, soon (several months) after the clinical onset of the disease. Unfortunately, the recent Statement of three scientific organisations from the USA proposed a reconsideration of the well-known classical stages, not going backward to know better the true early onset of the autoimmunity, but refining only the second part of the classical stages which are closer to the clinical onset of diabetes (when the β-cell mass/function is about 70% already irreversibly lost). In opposition with the above mentioned initiative, our effort has been devoted to the detection of earlier stages of diabetes which silently operate before the detection of the first islet autoantibodies (mainly proinsulin/insulin antibodies) which strangely was omitted in the new mentioned reclassification of preclinical stages of type 1 diabetes.

More than one century passed from the first proposed classification of diabetes in two phenotypes which survived in all the official classifications of WHO, despite the repeated suggestion that, in the light of the new biochemical, immunological and genetic data, the old black and white view on diabetes must be challenged. The time for a reclassification is now!