¿La prediabetes existe?

The cutoff levels for diagnosing diabetes mellitus (DM) were established because above these levels, the frequency of diabetic retinopathy (DR) increased. However, if DR is present but is below these thresholds, does the patient already have DM? The diagnostic plasma glucose levels at 120 minutes of the oral glucose tolerance test (OGTT) arose from studies by Pimas, Whitehall, and Bedford, which demonstrated that both DR and nephropathy occurred almost exclusively with values ​​of 200 mg/dL or higher. Subsequently, the fasting plasma glucose level was adapted to this parameter, establishing 126 mg/dL for diagnosis. The highest sensitivity and specificity for predicting the development of diabetic retinopathy (DR) in the studied populations (diagnosed by direct ophthalmoscopy or a single fundus photograph) is ≥126 mg/dL fasting and ≥200 mg/dL at 120 minutes of the oral glucose tolerance test (OGTT). Does this rule out the possibility that a patient with 122 mg/dL fasting and 189 mg/dL at 120 minutes could develop microangiopathy? In this regard, the Diabetes Prevention Program Research Group (DPP) detected DR in 7.9% of subjects with prediabetes (PDT2) after an average follow-up of 3.1 years, a figure that reached 14% 20 years after randomization. Likewise, confocal corneal microscopy shows that 40% of people with PDT2 present with neuropathy. In addition, a recent meta-analysis showed no statistically significant difference in the prevalence of distal polyneuropathy in patients with newly diagnosed diabetes mellitus (DM) versus those with type 2 diabetes (T2D) due to impaired glucose tolerance (IGT) plus impaired fasting glucose (IFG) [1,249 subjects / 4 studies / OR 1.24 (95% CI 0.67–2.31) / I² 50.12%]6. Furthermore, chronic kidney disease in T2D versus HbA1c <5% showed a hazard ratio of 1.08 (95% CI 1.02–1.14; P < 0.001)7. This demonstrates that all microvascular complications may already be present during T2D. In the macrovascular domain, the DECODE Study Group concluded that the relationship between mortality and blood glucose levels is continuous and lacks a defined biological threshold8. Similarly, DeFronzo notes that individuals with impaired glucose tolerance (IGT) and/or impaired fasting glucose (IFG) have a high risk of experiencing a cardiovascular event (CVD), which accounts for 80% of deaths in this group. These pathophysiological alterations are clearly expressed in subjects with IGT and/or IFG, where impaired β-cell function is observed, associated with dyslipidemia, hypertension, obesity, physical inactivity, insulin resistance, a procoagulant state, endothelial dysfunction, and inflammation Individual risk should be differentiated not only by glycemic and HbA1c levels, but also according to the patient's particular phenotype: from those with type 2 diabetes (T2D) at low risk of complications and progression to those at high risk due to metabolic syndrome and steatotic liver disease associated with metabolic dysfunction. In conclusion, there is a fundamental confusion regarding the diagnosis of T2D and diabetes mellitus (DM), an assertion supported by solid evidence that maintains the impossibility of dividing them into two different nosological entities.