Diabetes · For patients, families and doctors
Type 2 is the common answer, but about one in ten adults with diabetes has something else: slow-onset type 1 (LADA), a single-gene form (MODY), a damaged pancreas, a medicine, or a type 2 that behaves in a particular way. A wrong type is a wrong treatment. This check takes the history a diabetologist would take, adds any tests you already have, and tells you what it points to, which test would settle it, and what the answer would change.
A guide for you and your doctor, not a diagnosis. The type is settled by tests (antibodies, C-peptide, sometimes a gene test), not by a questionnaire. Answer what you know; leave the rest blank. Never change or stop insulin because of what this page says. Nothing you enter leaves this device.
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Caspian Healthcare reception: 89193 41154. Antibody and C-peptide tests are done at Caspian Diagnostic Centre in the same building.
| Step | Test | Reading it |
|---|---|---|
| 1 | Islet antibodies: GAD65 first, then IA-2 and ZnT8 if negative | Any positive: autoimmune diabetes. Onset at 30 or over with no insulin need for 6 months: LADA. About 10% of true type 1 is antibody negative, and one in ten of those is positive on a second antibody. |
| 2 | MODY features when antibody negative: onset under 35, a parent with diabetes, BMI under 30, C-peptide preserved | Run the Exeter MODY calculator; a probability above the local threshold goes to a gene panel. HNF1A and HNF4A: low-dose sulfonylurea. GCK: no treatment outside pregnancy. HNF1B: kidney cysts, check renal function. |
| 3 | C-peptide, random or stimulated, with a paired glucose, at 3 years or more from diagnosis | Under 200 pmol/L (0.6 ng/mL): insulin deficient, treat as type 1. 200 to 600: indeterminate, repeat in 6 to 12 months. Over 600 (1.8 ng/mL): type 2 or MODY. Early after diagnosis only the extremes are informative. |
| 4 | If the onset was ketoacidosis with negative antibodies | Ketosis-prone type 2 (A−β+ by the Aβ system): insulin now, reassess C-peptide at 3 to 6 months, half or more can stop insulin. Relapse is common; keep a sick-day plan. |
| 5 | Pancreatic disease: faecal elastase, imaging, fat-soluble vitamins | Type 3c: enzyme replacement with meals, insulin often needed, brittle sugars with glucagon deficiency, alcohol cessation, surveillance for pancreatic cancer in chronic pancreatitis. |
From the Indian INSPIRED study (Anjana 2020), with the Swedish names (Ahlqvist 2018) alongside. The formal clusters need HOMA2-B and HOMA2-IR from fasting C-peptide and glucose; this page approximates them from age, build, HbA1c, C-peptide and lipids, and says so.
| Pattern | Looks like | Watch for | Treatment leaning |
|---|---|---|---|
| SIDD | Younger, lean to normal build, HbA1c high at diagnosis, low C-peptide | Retinopathy and neuropathy; early tablet failure | Do not delay intensification; insulin or a GLP-1 receptor agonist early; check antibodies once |
| IROD (close to SIRD) | Obese, high C-peptide, acanthosis, high triglycerides, low HDL | Kidney disease, fatty liver, heart disease | Weight loss with real numbers, SGLT2 inhibitor and GLP-1 receptor agonist, metformin, pioglitazone in selected patients |
| CIRDD | Overweight with poor insulin output: resistance and deficiency together | Both microvascular and macrovascular disease | Combination therapy from the start; weight work and beta-cell support together |
| MARD | Older at diagnosis, mild hyperglycaemia, modest weight | Hypoglycaemia from over-treatment, frailty | Metformin, relaxed targets in the elderly, avoid sulfonylureas in the frail |
Immune destruction of the insulin cells. Any age, most often under 30. Lean or normal build, thirst and weight loss over weeks, often ketones. Antibody positive in 90%. Insulin from the start, for life.
Type 1 in slow motion, starting at 30 or over. Looks like type 2 for one to six years, then tablets fail. Antibody positive, no insulin needed in the first six months. Insulin early rather than late; sulfonylureas make it worse.
Insulin resistance and a pancreas that cannot keep up. Usually over 30, overweight or central fat, a parent with it, found on a routine test. Nine in ten Indian adults with diabetes. Comes in four patterns that behave differently.
One gene, passed parent to child. Diagnosed under 25 to 35, not obese, two or three generations, antibody negative, insulin still made. Often no treatment (GCK) or a tablet (HNF1A, HNF4A) instead of insulin.
Starts with ketoacidosis in an overweight adult, antibody negative. Insulin for weeks to months, then the pancreas recovers and insulin can often stop. Can relapse.
Chronic pancreatitis, fibrocalculous pancreatic diabetes, pancreatic surgery or cancer. Lean, upper abdominal pain, greasy stools, brittle sugars. Enzymes with meals, insulin, no alcohol.
Steroids most often; also some antipsychotics, transplant medicines, HIV medicines and cancer immunotherapy. Steroid diabetes may settle; checkpoint-inhibitor diabetes behaves like type 1 and is permanent.
Found in pregnancy, usually settles after delivery. Retest at 6 to 12 weeks, then every 1 to 3 years: about half develop type 2 within ten years. A high HbA1c early in pregnancy means diabetes that was already there.
The point weights behind the ranking are clinical judgement built on these sources; they are not a validated score, and the type 2 patterns are approximated without HOMA indices. Found an error? Write to info@caspianhealthcare.in.