A 58-year-old obese woman (BMI 32 kg/m²) from Delhi presents with a 2-year history of progressive fatigue and blurred vision. She reports no acute symptoms. Fasting blood glucose is 156 mg/dL, postprandial glucose 284 mg/dL, and HbA₁c 9.2%. C-peptide is 3.5 ng/mL (normal 0.8–3.1). Serum ketones are negative. She has no family history of diabetes. What is the most likely diagnosis?

Explanation

## Clinical Presentation Analysis **Key Point:** The insidious onset (2 years), obesity (BMI 32), elevated C-peptide (3.5 ng/mL), absence of ketosis, and gradual progression with microvascular complications (blurred vision) are characteristic of Type 2 diabetes mellitus. ## Diagnostic Differentiation: Type 1 vs Type 2 vs LADA | Feature | Type 1 DM | Type 2 DM | LADA | |---------|-----------|-----------|------| | **Age of onset** | Young (< 40 yrs) | Middle-aged/elderly (> 40 yrs) | Adults (> 30 yrs) | | **BMI** | Lean (< 25) | Obese (> 25) | Lean/normal | | **Onset** | Acute (days–weeks) | Insidious (months–years) | Insidious (years) | | **Presentation** | DKA, polyuria, polydipsia | Asymptomatic/microvascular complications | Gradual insulin requirement | | **C-peptide** | Undetectable (< 0.3 ng/mL) | Normal/elevated (> 1.0 ng/mL) | Low/detectable initially | | **Ketosis** | Present | Absent | Absent | | **Autoimmune markers** | GAD-65, IA-2, ZnT8 positive | Negative | Positive (GAD-65, IA-2) | | **Insulin requirement** | Immediate | Delayed (years) | Gradual (months–years) | **High-Yield:** C-peptide > 1.0 ng/mL indicates preserved endogenous insulin secretion. In Type 2 DM, the pancreas still produces insulin but cells are resistant to its action. This patient's C-peptide of 3.5 ng/mL rules out Type 1 DM (where it is undetectable). ## Pathophysiology of Type 2 DM 1. Genetic predisposition + obesity → insulin resistance 2. Pancreatic β-cells initially compensate with ↑ insulin secretion 3. Over time, β-cell dysfunction develops (progressive loss of glucose-stimulated insulin secretion) 4. Fasting and postprandial hyperglycaemia emerge 5. Microvascular complications (retinopathy, nephropathy, neuropathy) develop insidiously **Clinical Pearl:** Blurred vision in this patient likely reflects early diabetic retinopathy, a common microvascular complication of poorly controlled Type 2 DM. The 2-year history allows time for these complications to develop. ## Why Not LADA? **Mnemonic: LADA = "Lazy" Type 1** — Latent Autoimmune Diabetes in Adults. LADA is a slowly progressive autoimmune form of diabetes that presents in adults > 30 years. While this patient is 58 years old (within LADA range), the key distinguishing features are: - **Obesity:** LADA patients are typically lean; this patient is obese (BMI 32) - **Autoimmune markers:** LADA is GAD-65 or IA-2 positive; this patient has no mention of seropositivity - **C-peptide trajectory:** LADA shows gradual decline in C-peptide over years; this patient's C-peptide is still elevated (3.5 ng/mL) - **Insulin requirement:** LADA requires insulin within 6 years of diagnosis; Type 2 DM may be managed with oral agents for years **Warning:** Do not confuse LADA with Type 2 DM. LADA is autoimmune (like Type 1) but presents slowly (like Type 2). The absence of autoimmune serology and the presence of obesity make Type 2 DM the diagnosis here.