Hyperosmolar hyperglycaemic state as a stroke cause or stroke mimic: an illustrative case and review of literature.

Hyperosmolar hyperglycaemic state (HHS) is a life-threatening metabolic complication of type 2 diabetes (T2DM) that often presents with neurological symptoms. A 74-year-old man with known T2DM presented to the emergency department with collapse, left-sided weakness and slurred speech (National Institutes of Health Stroke Scale (NIHSS) 3) and a biochemical profile consistent with HHS. When he further deteriorated (NIHSS 20), he was managed for concurrent ischaemic stroke. All his symptoms fully resolved after 24 hours, which coincided with establishment of normoglycaemia. Subsequent magnetic resonance imaging (MRI) of the head revealed a tiny parietal lobe infarct. Two further cases of HHS mimicking ischaemic stroke have been reported with symptoms and imaging findings resolving with treatment of HHS. Our case demonstrates how HHS can also accentuate symptoms of a minor stroke, highlighting the importance of excluding ischaemic stroke in HHS patients with neurological dysfunction. We recommend consideration of early MRI and/or computed tomography angiography in this cohort, especially in those appropriate for intervention.

Measurement of Peak C-Peptide at Diagnosis Informs Glycemic Control but not Hypoglycemia in Adults With Type 1 Diabetes.

CONTEXT: High-residual C-peptide in longer-duration type 1 diabetes (T1D) is associated with fewer hypoglycemic events and reduced glycemic variability. Little is known about the impact of C-peptide close to diagnosis. OBJECTIVE: Using continuous glucose monitoring (CGM) data from a study of newly diagnosed adults with T1D, we aimed to explore if variation in C-peptide close to diagnosis influenced glycemic variability and risk of hypoglycemia. METHODS: We studied newly diagnosed adults with T1D who wore a Dexcom G4 CGM for 7 days as part of the Exercise in Type 1 Diabetes (EXTOD) study. We examined the relationship between peak stimulated C-peptide and glycemic metrics of variability and hypoglycemia for 36 CGM traces from 23 participants. RESULTS: For every 100 pmol/L-increase in peak C-peptide, the percentage of time spent in the range 3.9 to 10 mmol/L increased by 2.4% (95% CI, 0.5-4.3), P = .01) with a reduction in time spent at level 1 hyperglycemia (> 10 mmol/L) and level 2 hyperglycemia (> 13.9 mmol/L) by 2.6% (95% CI, -4.9 to -0.4, P = .02) and 1.3% (95% CI, -2.7 to -0.006, P = .04), respectively. Glucose levels were on average lower by 0.19 mmol/L (95% CI, -0.4 to 0.02, P = .06) and SD reduced by 0.14 (95% CI, -0.3 to -0.02, P = .02). Hypoglycemia was not common in this group and no association was observed between time spent in hypoglycemia (P = .97) or hypoglycemic risk (P = .72). There was no association between peak C-peptide and insulin dose-adjusted glycated hemoglobin A1c (P = .45). CONCLUSION: C-peptide is associated with time spent in the normal glucose range and with less hyperglycemia, but not risk of hypoglycemia in newly diagnosed people with T1D.