Different diabetes

In the 2nd century AD, Aretaeus Cappadocian noted that some people with diabetes were thin, and others overweight. late 19th Lancereaux called these diabète maigre gros.1 Since then, have been named juvenile maturity-onset diabetes, insulin-dependent non-insulin-dependent type 1 2 diabetes. But of course there are not just two types – may be thousands. many cases, cause a person's is multifactorial. Sometimes unclear. Even when it clear, wrongly recorded.2 Don’t miss less common variants especially those require different treatment or an unexpected course. Some listed in Box 1. Harry was 16 years old he developed polyuria polydipsia. His mother had as did her father six more relatives. Harry's mother…said: ‘we’d actually taken drawn-up family tree, but they didn’t do anything about it, said: “He's 1”.’ started on insulin. He great difficulty controlling his blood glucose: ‘The glucose levels all over place…I get any warnings, nasty, one minute I’d kicking football around next flat out floor.’ often unconscious at night. Seven months after diagnosis islet-related antibody test proved negative consultant still insisted suspected young (MODY). She found expert website www.diabetesgenes.org arranged which confirmed mutation HNF1A, MODY. HNF1A mutations 50% cases monogenic It estimated 1–2% MODY.3, 4 insulin stopped small dose gliclazide. life transformed from being unsafe to drive failing college passed exams got place veterinary college. A detailed account published this journal recently.5 There 31,615 children National Paediatric Diabetes Audit (England Wales) 2020–21 only 162 (0.5%) should more.6 Do you patient possible MODY? Use MODY probability calculator (https://www.diabetesgenes. org/exeter-diabetes-app/ModyCalculator).4 37-year-old man, previously well, admitted two-day history diarrhoea vomiting. On examination lucid low spirits’; pulse 102 beats/min, respiratory rate 18 breaths/min, pressure 100/58mmHg, otherwise unremarkable. tests showed diabetic ketoacidosis 74.6mmol/L (1342mg/dl), HbA1c 6.2% (44mmol/mol). C-peptide antibodies (ICA, IAA GAD) negative. recovered standard long-term therapy.7 This man fulminant first described Japan where accounts for 20% newly diagnosed acute-onset diabetes.8 seen other East Asian populations occasionally Westerners.9 thought viral infection genetic susceptibility triggers rapid immunological process destroys beta-cells damages exocrine pancreas cells. Fulminant occur patients treated immune checkpoint inhibitors.10 70% hyperglycaemia preceded by flu-like symptoms gastrointestinal symptoms. can pregnancy soon delivery. Other frequent concomitants absent raised serum pancreatic enzyme (98% patients).11 ‘Once disease suspected, must immediately, Otherwise, death likely within 24 h. All medical practitioners remember extremely rapidly progressing does exist, pay special attention overlook it.’12 Islet cells suffer autoimmune damage age. LADA, also known slowly evolving immune-mediated adults, affects 12% adult-onset Diagnostic criteria included age >30 years, family, weight normal slightly overweight, measurable C-peptide, GAD positive, needing first, although needed eventually. Oral agents non-insulin treatments used initially, such metformin. The benefits use start preserve beta-cell function yet confirmed. SGLT2 inhibitors help risk developing ketoacidosis. suggested monitored, if has increased reduce hyperglycaemia. Patient clinician education important illness surgery, example, precipitate management strategy consensus statement international panel.13 well forties Central African ethnicity no polydipsia months. fell 106kg 91kg. admission looked plasma 40mmol/L (720mg/dl) marked ketosis acidosis. fluid replacement Islet-related discharged total 82 units daily 14–20 week later. At three experiencing hypoglycaemia despite further reduction. sitagliptin started.14 ketosis-prone Flatbush type-J 1.5 phasic prairie ethnicity, example African-Americans, affect ethnic groups. sub-Saharan Africa up 15% new presenting hospital. presents relatively short history, who overweight level usually high ketoacidosis; causes fall glucose, stop days weeks, sometimes glucose-lowering treatment. They episodes short-term treatment.15 UK community study among 206 aged <45 review diagnosis, targeted testing. Type 33%, 54%, subtypes 13%. latter comprised 9% 3% (from five families) 1% mitochondrial Including families tested result project ‘led minimum population prevalence 84 (95% CI 31–136) per million HNF1A-MODY.’16 variants. Remember them see both existing almost certainly unusual every clinic. Misdiagnosis lead wrong failure recognise potential dangers. much misery. Always record Listen their family. Many need An accurate available. test! comes fast kill fast. Beware very glucose. Autoimmune LADA. Ketosis-prone fluctuates mandating all. Ketosis recur.