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Diabetes mellitus is a syndrome of various genetic and environmental etiologies. The hyperglycemia and its associated metabolic, functional and pathological sequelae apparently have different mechanisms, depending on the several entities encountered. Two major clinical presentations of diabetes are reviewed in this chapter and their genetic and pathogenetic characteristics are described. Patients with diabetes will eventually develop micro- and macro-vascular complications, making their lives increasingly uncomfortable and distressing. A short report on these grave afflictions, their pathogenesis and course of disease has been given. The relationship between diabetic control and complications is also discussed. Although a lot of progress in understanding diabetes and its therapy has been made in the last six decades, a great deal is still left for future clinical and basic research to accomplish.

We compared concentrations of antithrombin III (AT-III) in plasma, as determined by an immunological method and by a functional thrombin inhibition method, in the presence of heparin in 160 blood samples from Type I diabetics. Although the correlation was highly significant (P less than 0.001) between the results obtained by the two methods, our data demonstrated that results by the thrombin inhibition assay, 121 (SD 15)%, expressed as percentages of the results for a normal plasma pool, were significantly (P less than 0.001) higher than by the immunoreactive method, 104 (SD 15)%, indicating an overestimation of functionally active AT-III. Concentrations of functionally active AT-III determined by a factor Xa inhibition assay, 105 (SD 13)%, were in the same range as immunoreactive AT-III. Addition of IgG antiserum to normal pooled plasma quenched only about 90% of the AT-III activity determined by the thrombin inhibition assay, but all of the AT-III activity determined by a factor Xa inhibition assay. These results demonstrate that the factor Xa inhibition assay is more specific for the determination of AT-III than the thrombin inhibition assay. We suggest that the high concentrations of heparin cofactor II, 117 (SD 17)%, might have caused an overestimation of AT III in this group of patients with diabetes Type I, and should not be overlooked in other clinical situations.

Lp(a) lipoprotein in diabetes type I