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Aims

Hypoglycaemia causes QT‐interval prolongation and appears pro‐arrhythmogenic. Salbutamol, a β2‐adrenoreceptor agonist also causes QT‐interval prolongation. We hypothesized that the magnitude of electrophysiological changes induced by salbutamol and hypoglycaemia might relate to each other and that salbutamol could be used as a non‐invasive screening tool for predicting an individual's electrophysiological response to hypoglycaemia.

Methods

Eighteen individuals with Type 1 diabetes were administered 2.5 mg of nebulized salbutamol. Participants then underwent a hyperinsulinaemic–hypoglycaemic clamp (2.5 mmol/l for 1 h). During both experiments, heart rate and serum potassium (and catecholamines during the clamp) were measured and a high‐resolution electrocardiogram (ECG) was recorded at pre‐set time points. Cardiac repolarization was measured by QT‐interval duration adjusted for heart rate (QTc), T‐wave amplitude (Tamp), T‐peak to T‐end interval duration (TpTend) and T‐wave area symmetry (Tsym). The maximum changes vs. baseline in both experiments were assessed for their linear dependence.

Results

Salbutamol administration caused QTc and TpTend prolongation and a decrease in Tamp and Tsym. Hypoglycaemia caused increased plasma catecholamines, hypokalaemia, QTc and TpTend prolongation, and a decrease in Tamp and Tsym. No significant correlations were found between maximum changes in QTc [r = 0.15, 95% confidence interval (95% CI) ?0.341 to 0.576; P = 0.553), TpTend (r = 0.075, 95% CI ?0.406 to 0.524; P = 0.767), Tsym (r = 0.355, 95% CI ?0.132 to 0.706; P = 0.149) or Tamp (r = 0.148, 95% CI ?0.347 to 0.572; P = 0.558) in either experiment.

Conclusions

Both hypoglycaemia and salbutamol caused pro‐arrhythmogenic electrophysiological changes in people with Type 1 diabetes but were not related in any given individual. Salbutamol does not appear useful in assessing an individual's electrophysiological response to hypoglycaemia.
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2.
Background

Parathyroidectomy is the treatment of choice in primary hyperparathyroidism (PHPT). Following surgery, significant changes in bone and mineral metabolism may follow, but routine magnesium monitoring is not standard practice. The occurrence of significant clinical events linked to hypomagnesaemia in 3 patients after parathyroidectomy led to our evaluation of magnesium levels after surgery for PHPT.

Methods

Serum magnesium levels before and after parathyroidectomy for PHPT were prospectively evaluated in a single centre over a year. The incidence and severity of hypomagnesaemia and its correlation with other biochemical variables were assessed.

Results

A total of 138 patients underwent parathyroidectomy for PHPT. Pre-operative and day 1 post-operative serum magnesium levels were available in 57/138 (41.3%) and 99/138 (71.7%) patients, respectively. Serum magnesium decreased significantly after surgery (mean ± SD of 0.85 ± 0.08 and 0.75 ± 0.11 mmol/L, respectively, p < 0.001). On the day after parathyroidectomy, 31/99 (31.3%) patients had hypomagnesaemia (<0.70 mmol/L); in 3 of whom it was severe (<0.50 mmol/L). Patients with hypomagnesaemia had lower pre-operative magnesium (mean ± SD of 0.78 ± 0.06 and 0.87 ± 0.07 mmol/L, p < 0.001), higher pre-operative calcium [median (IQR) of 2.83 (2.71–2.99) and 2.71 (2.63–2.80) mmol/L, p = 0.001] and higher post-operative calcium [median (IQR) of 2.41 (2.30–2.51) and 2.35 (2.28–2.43) mmol/L, p = 0.046] compared to those with normomagnesaemia. In addition, these patients demonstrated higher drop in calcium levels after surgery (0.44 ± 0.20 and 0.35 ± 0.18 mmol/L, p = 0.033). Magnesium levels after surgery correlated positively with pre-operative magnesium (r = 0.561, p < 0.001) and post-operative PTH (r = 0.210, p = 0.037) and negatively with pre-operative adjusted calcium (r = − 0.389, p < 0.001).

Conclusions

Serum magnesium decreased significantly following parathyroidectomy for PHPT and nearly a third of patients developed post-operative, mostly mild hypomagnesaemia. Whilst routine serum magnesium measurements could facilitate prompt recognition and treatment of this electrolyte disturbance, further research needs to establish the clinical importance of mild hypomagnesaemia in these clinical settings and, if indicated, to devise optimal treatment strategies.

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