Despite many recent advances, the management of patients with Cushing's disease continues to be challenging. Cushing's syndrome is a complex metabolic disorder that is a result of excess glucocorticoids. Excluding the exogenous causes, adrenocorticotropic hormone–secreting pituitary adenomas account for nearly 70% of all cases of Cushing's syndrome. The suspicion, diagnosis, and differential diagnosis require a logical systematic approach with attention paid to key details at each investigational step. A diagnosis of endogenous Cushing's syndrome is usually suspected in patients with clinical symptoms and confirmed by using multiple biochemical tests. Each of the biochemical tests used to establish the diagnosis has limitations that need to be considered for proper interpretation. Although some tests determine the total daily urinary excretion of cortisol, many others rely on measurements of serum cortisol at baseline and after stimulation (e.g., after corticotropin-releasing hormone) or suppression (e.g., dexamethasone) with agents that influence the hypothalamic-pituitary-adrenal axis. Other tests (e.g., measurements of late-night salivary cortisol concentration) rely on alterations in the diurnal rhythm of cortisol secretion. Because more than 90% of the cortisol in the circulation is protein bound, any alteration in the binding proteins (transcortin and albumin) will automatically influence the measured level and confound the interpretation of stimulation and suppression data, which are the basis for establishing the diagnosis of Cushing's syndrome. Although measuring late-night salivary cortisol seems to be an excellent initial test for hypercortisolism, it may be confounded by poor sampling methods and contamination. Measurements of 24-hour urinary free-cortisol excretion could be misleading in the presence of some pathological and physiological conditions. Dexamethasone suppression tests can be affected by illnesses that alter the absorption of the drug (e.g., malabsorption, celiac disease) and by the concurrent use of medications that interfere with its metabolism (e.g., inducers and inhibitors of the P450 enzyme system). In this review, the authors aim to review the pitfalls commonly encountered in the workup of patients suspected to have hypercortisolism. The optimal diagnosis and therapy for patients with Cushing's disease require the thorough and close coordination and involvement of all members of the management team.

ObjectiveWe compared the cost-effectiveness of two inpatient diabetes care models: one offered by a specialized diabetes team (SDT) versus a primary service team (PST).Research design and methodsWe retrospectively evaluated 756 hospital admissions of patients with diabetes to non-critical care units over 6 months. Out of 392 patients who met the eligibility criteria, 262 were matched 1:1 based on the mean of the initial four blood glucose (BG) values after admission. Primary outcomes were 30-day readmission rate and frequency, hospital length of stay (LOS) and estimated hospital cost. Secondary outcomes included glycemic control and BG variability.ResultsDiabetes complexity and in-hospital complications were significantly higher among patients treated by SDT versus PST. Thirty-day readmission rate to medical services was lower by 30.5% in the SDT group versus the PST group (P<0.001), while 30-day readmission rate to surgical services was 5% higher in the SDT group versus the PST group (P<0.05), but frequency of 30-day readmissions was lower (1.1 vs 1.6 times, P<0.05). LOS in medical services was not different between the two groups, but it was significantly longer in surgical services in SDT (P<0.05). However, LOS was significantly lower in patients who were seen by SDT during the first 24 hours of admission compared with those who were seen after that (4.7 vs 6.1 days, P<0.001). Compliance to follow-up was higher in the SDT group. These changes were translated into considerable cost saving.ConclusionsInpatient diabetes management by an SDT significantly reduces 30-day readmission rate to medical services, reduces inpatient diabetes cost, and improves transition of care and adherence to follow-up. SDT consultation during the first 24 hours of admission was associated with a significantly shorter hospital LOS.

SummaryRadioactive iodine (RAI) ablation is a beneficial, adjuvant therapy for the management of differentiated thyroid cancer (DTC) after thyroidectomy. The goal of RAI is to destroy remnant thyroid and microscopic cancerous tissue. Radioactive iodine uptake is enhanced by elevating TSH levels and initiating a low iodine diet (LID) prior to ablation. An ideal LID should preferably not exceed 50 mcg/day of dietary iodine for 1-2 weeks, although the duration may be shortened to a week with a structured patient education programme. A pre-ablation spot urinary iodine concentration (UIC) of <100 mcg/l and/or a urinary iodine to creatinine ratio (UICR) of <100 mcg/gCr would support an adequate LID preparation. Hyponatraemia, most likely due to iatrogenic hypothyroidism, is a potential side effect associated with LID and occurs during and a few days after the LID. Although the overall incidence of hyponatraemia is low, patients at high risk (older age, female sex, use of thiazide diuretics) may benefit from serum sodium monitoring. The existing evidence on the impact of LID on RAI ablation has been largely inconsistent due to retrospective study designs and the lack of an objective measurement of urinary iodine levels. Future large prospective randomized control trials are needed to elucidate and confirm the crucial role of LID in achieving successful RAI ablation and greater disease-free survival in DTC.

Measuring intra-abdominal fat identifies a subset of patients with worse prognosis in pancreatic cancer.