Summary Background:  Patients with diabetes mellitus are at an increased risk of thyroid disease. The frequency of thyroid dysfunction in diabetic patients is higher than that of the general population and up to a third of patients with type‐1 diabetes (T1DM) ultimately develop thyroid dysfunction. Unrecognised thyroid dysfunction may impair metabolic control and add to cardiovascular disease risk in diabetic patients. Aims:  Our aims were to review the current literature on the association between thyroid dysfunction and diabetes mellitus, to highlight relevant clinical implications, and to examine present thyroid disease screening strategies in routine diabetes care. Results:  The pleiotropic effects of thyroid hormones on various metabolic processes are now better understood. Uncontrolled hyperthyroidism in diabetic patients may trigger hyperglycaemic emergencies while recurrent hypoglycaemic episodes have been reported in diabetic patients with hypothyroidism. Furthermore, thyroid dysfunction may amplify cardiovascular disease risk in diabetic patients through inter‐relationships with dyslipidaemia, insulin resistance and vascular endothelial dysfunction. However, the significance of subclinical degrees of thyroid dysfunction remains to be clarified. While these developments have implications for diabetic patients a consensus is yet to be reached on optimal thyroid screening strategies in diabetes management. Conclusions:  The increased frequency of thyroid dysfunction in diabetic patients and its likely deleterious effects on cardiovascular and metabolic function calls for a systematic approach to thyroid disease screening in diabetes. Routine annual thyroid testing should be targeted at diabetic patients at risk of thyroid dysfunction such as patients with T1DM, positive thyroid autoantibodies or high‐normal TSH concentrations.

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Background: Short synacthen tests (SSTs) are frequently performed in medical inpatients with suspected adrenocortical insufficiency. The utility of a random or baseline serum cortisol in this setting is unclear. We determined random cortisol thresholds that safely preclude SSTs in acute medical admissions. Methods: We analysed SSTs in acute non-critically ill general medical patients (n ¼ 166, median age 66, range 15-94 y; men 48%, women 52%). The SST was defined according to the 30-min cortisol as 'pass' (.550 nmol/L) or 'fail' (550 nmol/L). Receiver operating characteristics (ROC) curves were generated to determine the predictive value of the basal cortisol for a failed SST. Results: Of 166 SSTs, a pass was seen in 127 (76.5%) tests, while 39 (23.5%) tests failed the SST. ROC curves showed that no single cut-off point of the baseline cortisol was adequately both sensitive and specific for failing the SST despite a good overall predictive value (area under curve 0.94; 95% confidence interval 0.89-0.98). A basal cortisol ,420 nmol/L had 100% sensitivity and 54% specificity for failing the SST, while a basal cortisol ,142 nmol/L had 100% specificity and 35% sensitivity. Restricting the SST to patients with a basal cortisol ,420 nmol/L would have prevented 44% of SSTs while correctly identifying all patients who failed the SST. Conclusion: A baseline serum cortisol may prevent unnecessary SSTs in medical inpatients with suspected adrenocortical insufficiency. However, SSTs are still indicated in patients with random cortisol ,420 nmol/L, or where the suspicion of adrenal insufficiency is compelling.