Acute phase reactant dynamics and incidence of microvascular dysfunctions in type 2 diabetes mellitus

BACKGROUND: Acute Phase Reactants (APRs) have a wide range of activities that contribute to host defense. The aim of this report was to evaluate the dynamics and magnitude of these proteins in various microvascular complications in diabetes mellitus (DM). We also sought to assess the predictive values of APRs and other clinical variables for microvascular complications in DM. METHODS: This was a case control study carried out in 200 Nigerian subjects with type 2 DM and 100 sex and age matched healthy controls. The studied APRs included C-reactive protein, beta 2 microglobulin, fibrinogen and lipoprotein (a). RESULTS: The mean values of the APRs were significantly higher in type 2 DM compared with the controls and were observed in higher concentrations in those with microvascular complications, except beta 2 microglobulin. Presence of microvascular complications was observed in those with dilated fundus examination (retinopathy), symptom score of 3.0 (neuropathy), urea and creatinine levels above 50mg% and 1.5mg%, respectively, with significant proteinuria (nephropathy). Significant increase in mean ± SEM values of lipoprotein (a) was observed in diabetic retinopathy in comparison with those without complications (25.76 ± 1.13 mg/dl vs. 22.37 ± 0.73 mg/dl, p = 0.005). Elevated C-reactive protein was observed in diabetic neuropathy in comparison with those without complications (11.43 ± 2.33 u/ml vs. 8.30 ± 1.15 u/ml, p = 0.048). Increased beta 2 microglobulin levels were observed in patients with diabetic foot ulcers in comparison with those without complications (3.04 ± 0.51 mg/dl vs. 2.54 ± 0.14 mg/dl, p = 0.049). Circulating levels of Lipoprotein (a) predicted retinopathy in DM with both good and poor long-term glycemic control while duration of DM predicted the occurrence of foot ulcers.. CONCLUSIONS: Increased level of APRs was associated with a number of microvascular complications and may play a role in the pathogenesis.