Pheochromocytomas (PCCs) are rare catecholamine producing neuroendocrine tumors. The majority of these tumors (85 %) arise from the adrenal medulla. Those arising from the extra-adrenal neural ganglia are called paragangliomas (PGLs). Paroxysmal hypertension with sweating, headaches and palpitation are the usual presenting features of PCCs/ PGLs. Gene mutations are reported in 32-79 % of cases, making genetic screening mandatory in all the cases. The malignancy rates are 10-15 % for PCCs and 20-50 % for PGLs. Measurement of plasma or 24-hour urinary fractionated metanephrines is the best biochemical diagnostic test. Computed tomography or magnetic resonance imaging has high sensitivity (90-100 %) and reasonable specificity (70-90 %) for the anatomical localization. The functionality is assessed by different radionuclide imaging modalities such as metaiodobenzylguanidine (MIBG) scintigraphy, positron emission tomography or single photon emission computed tomography. The only modality of curative treatment is tumor excision. Proper peri-operative management improves the surgical outcomes. Annual follow up with clinical and biochemical assessment is recommended in all the cases after treatment. Children, pregnant women and older people have higher morbidity and mortality risk. De-bulking surgery, chemotherapy, radiotherapy, molecular agents like sunitinib and everolimus, radionuclide agents and different ablation procedures may be useful in the palliation of inoperable/metastatic disease. An update on the diagnostic evaluation and management of PCCs and PGLs is presented here.

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In the recent years, non-alcoholic fatty liver disease (NAFLD) has emerged as the commonest cause of chronic liver disease in the developed world. The global epidemic of obesity secondary to physical inactivity and adverse food habits accounts for the alarming rise in NAFLD. Metabolic syndrome plays a major role in the pathogenesis of both NAFLD and type 2 diabetes mellitus (T2DM). Whilst most cases of NAFLD remain asymptomatic with only hepatic steatosis, about 30 % progress to non-alcoholic steatohepatitis with chronic liver inflammation that can lead on to fibrosis, cirrhosis, liver failure, and hepatocellular carcinoma. Because of the similar pathogenesis shared between T2DM and NAFLD, T2DM occurs as an important complication in many cases of NAFLD, and many cases of T2DM are further complicated by NAFLD. Rapid progression and increased complications of the individual diseases is the end result of this dual coexistence. Diagnosis of NAFLD relies upon hepatic imaging, serum biochemical markers, and liver biopsy. As in T2DM, the most important management option for patients with NAFLD is lifestyle changes targeted at weight reduction. Other treatment options include insulin sensitizers (metformin and pioglitazone), vitamin E, incretin mimetics, omega-3 fatty acids, cholesterol lowering agents, orlistat, and bariatric surgery. The clinical spectrum, patho-physiological features and therapeutic options of NAFLD share many things in common with T2DM and therefore, this review is to highlight the diabetologist's perspective of the disease.

Diagnosis of Cushing's syndrome (CS) and identification of the aetiology of hypercortisolism can be challenging. The Endocrine Society clinical practice guidelines recommends one of the four tests for initial screening of CS, namely, urinary-free cortisol, late night salivary cortisol, overnight dexamethasone suppression test or a longer low-dose dexamethasone suppression test, for 48 hours. Confirmation and localisation of CS requires additional biochemical and radiological tests. Radiological evaluation involves different imaging modalities including MRI with or without different radio-nuclear imaging techniques. Invasive testing such as bilateral inferior petrosal sinus sampling may be necessary in some patients for accurate localisation of the cause for hypercortisolism. This best practice review discusses a practical approach for the diagnostic evaluation of CS with a brief discussion on differential diagnoses, and cyclical CS, to enhance the skills of clinicians and laboratory personnel.

Although the dysglycemic effects of systemic glucocorticoid therapy are well known, the effect of inhaled corticosteroids (ICS) on carbohydrate metabolism is still a subject of debate. The systemic bioavailability of ICS is claimed to be minimal and the side effects negligible. However, some large retrospective cohort studies showed a definite association between ICS use and incident diabetes or worsening glycemic control in pre-existing diabetes. There are no professional-body recommended guidelines on the diagnosis and management of steroid-induced diabetes for the general population. This review aims to evaluate the systemic dysglycemic effect of ICS treatment and to propose a management algorithm.

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Type 2 diabetes mellitus (T2DM) is a progressive disease associated with significant morbidity and mortality. There is good evidence that intensive glycemic control reduces the development and progression of complications in patients with diabetes. In order to achieve glycemic targets, patients often require a combination of oral therapy and/or insulin in addition to lifestyle modification. Unfortunately many currently available therapies for T2DM are associated with weight gain and hypoglycemia resulting in poor compliance and subsequent worsening glycemic control. Glucagon like peptide-1 (GLP-1) is an incretin hormone secreted from the small intestine that lowers fasting and postprandial glucose through multiple mechanisms including glucose-dependent insulin secretion, reduction of glucagon secretion, delaying gastric emptying and increased satiety. Liraglutide is a long acting GLP-1 mimetic that is administered once a day by subcutaneous injection and is now licensed for the treatment of T2DM. Phase 3 clinical trials have demonstrated beneficial effects on glycemic control and weight with liraglutide therapy. Within this article, we provide an overview of pharmacology, efficacy, safety and patient experience on liraglutide in the management of T2DM.

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