Nutritional strategies for correcting low glucose values in patients with postbariatric hypoglycaemia: A randomized controlled three-arm crossover trial.

AIM To evaluate the efficacy of nutritional hypoglycaemia correction strategies in postbariatric hypoglycaemia (PBH) after Roux-en-Y gastric bypass (RYGB). MATERIALS AND METHODS In a randomized, controlled, three-arm crossover trial, eight post-RYGB adults (mean [SD] 7.0 [1.4] years since surgery) with PBH ingested a solid mixed meal (584 kcal, 85 g carbohydrates, 21 g fat, 12 g protein) to induce hypoglycaemia on three separate days. Upon reaching plasma glucose of less than 3.0 mmol/L, hypoglycaemia was corrected with 15 g of glucose (G15), 5 g of glucose (G5) or a protein bar (P10, 10 g of protein) in random order. The primary outcome was percentage of time spent in the target plasma glucose range (3.9-5.5 mmol/L) during 40 minutes after correction. RESULTS Postcorrection time spent in the target glucose range did not differ significantly between the interventions (P = .161). However, postcorrection time with glucose less than 3.9 mmol/L was lower after G15 than P10 (P = .007), whereas time spent with glucose more than 5.5 mmol/L, peak glucose and insulin 15 minutes postcorrection were higher after G15 than G5 and P10 (P < .001). Glucagon 15 minutes postcorrection was higher after P10 than after G15 and G5 (P = .002 and P = .003, respectively). G15 resulted in rebound hypoglycaemia (< 3.0 mmol/L) in three of eight cases (38%), while no rebound hypoglycaemia occurred with G5 and P10. CONCLUSIONS Correcting hypoglycaemia with 15 g of glucose should be reconsidered in post-RYGB PBH. A lower dose appears to sufficiently increase glucose levels outside the critical range in most cases, and complementary nutrients (e.g. proteins) may provide glycaemia-stabilizing benefits. REGISTRATION NUMBER OF CLINICAL TRIAL NTC05250271 (ClinicalTrials.gov)

Nutritional strategies for correcting low glucose values in patients with postbariatric hypoglycaemia: A randomized controlled three‐arm crossover trial

AimTo evaluate the efficacy of nutritional hypoglycaemia correction strategies in postbariatric hypoglycaemia (PBH) after Roux‐en‐Y gastric bypass (RYGB).Materials and methodsIn a randomized, controlled, three‐arm crossover trial, eight post‐RYGB adults (mean [SD] 7.0 [1.4] years since surgery) with PBH ingested a solid mixed meal (584 kcal, 85 g carbohydrates, 21 g fat, 12 g protein) to induce hypoglycaemia on three separate days. Upon reaching plasma glucose of less than 3.0 mmol/L, hypoglycaemia was corrected with 15 g of glucose (G15), 5 g of glucose (G5) or a protein bar (P10, 10 g of protein) in random order. The primary outcome was percentage of time spent in the target plasma glucose range (3.9‐5.5 mmol/L) during 40 minutes after correction.ResultsPostcorrection time spent in the target glucose range did not differ significantly between the interventions (P = .161). However, postcorrection time with glucose less than 3.9 mmol/L was lower after G15 than P10 (P = .007), whereas time spent with glucose more than 5.5 mmol/L, peak glucose and insulin 15 minutes postcorrection were higher after G15 than G5 and P10 (P < .001). Glucagon 15 minutes postcorrection was higher after P10 than after G15 and G5 (P = .002 and P = .003, respectively). G15 resulted in rebound hypoglycaemia (< 3.0 mmol/L) in three of eight cases (38%), while no rebound hypoglycaemia occurred with G5 and P10.ConclusionsCorrecting hypoglycaemia with 15 g of glucose should be reconsidered in post‐RYGB PBH. A lower dose appears to sufficiently increase glucose levels outside the critical range in most cases, and complementary nutrients (e.g. proteins) may provide glycaemia‐stabilizing benefits.Registration number of clinical trialNTC05250271 (ClinicalTrials.gov)

Clinical and genetic characteristics of late-onset Huntington's disease

Background: The frequency of late-onset Huntington's disease (&gt;59 years) is assumed to be low and the clinical course milder. However, previous literature on late-onset disease is scarce and inconclusive. Objective: Our aim is to study clinical characteristics of late-onset compared to common-onset HD patients in a large cohort of HD patients from the Registry database. Methods: Participants with late- and common-onset (30–50 years)were compared for first clinical symptoms, disease progression, CAG repeat size and family history. Participants with a missing CAG repeat size, a repeat size of ≤35 or a UHDRS motor score of ≤5 were excluded. Results: Of 6007 eligible participants, 687 had late-onset (11.4%) and 3216 (53.5%) common-onset HD. Late-onset (n = 577) had significantly more gait and balance problems as first symptom compared to common-onset (n = 2408) (P &lt;.001). Overall motor and cognitive performance (P &lt;.001) were worse, however only disease motor progression was slower (coefficient, −0.58; SE 0.16; P &lt;.001) compared to the common-onset group. Repeat size was significantly lower in the late-onset (n = 40.8; SD 1.6) compared to common-onset (n = 44.4; SD 2.8) (P &lt;.001). Fewer late-onset patients (n = 451) had a positive family history compared to common-onset (n = 2940) (P &lt;.001). Conclusions: Late-onset patients present more frequently with gait and balance problems as first symptom, and disease progression is not milder compared to common-onset HD patients apart from motor progression. The family history is likely to be negative, which might make diagnosing HD more difficult in this population. However, the balance and gait problems might be helpful in diagnosing HD in elderly patients