International scientific experts in food, nutrition, dietetics, endocrinology, physical activity, paediatrics, nursing, toxicology and public health met in Lisbon on 2–4 July 2017 to develop a Consensus on the use of low- and no-calorie sweeteners (LNCS) as substitutes for sugars and other caloric sweeteners. LNCS are food additives that are broadly used as sugar substitutes to sweeten foods and beverages with the addition of fewer or no calories. They are also used in medicines, health-care products, such as toothpaste, and food supplements. The goal of this Consensus was to provide a useful, evidence-based, point of reference to assist in efforts to reduce free sugars consumption in line with current international public health recommendations. Participating experts in the Lisbon Consensus analysed and evaluated the evidence in relation to the role of LNCS in food safety, their regulation and the nutritional and dietary aspects of their use in foods and beverages. The conclusions of this Consensus were: (1) LNCS are some of the most extensively evaluated dietary constituents, and their safety has been reviewed and confirmed by regulatory bodies globally including the World Health Organisation, the US Food and Drug Administration and the European Food Safety Authority; (2) Consumer education, which is based on the most robust scientific evidence and regulatory processes, on the use of products containing LNCS should be strengthened in a comprehensive and objective way; (3) The use of LNCS in weight reduction programmes that involve replacing caloric sweeteners with LNCS in the context of structured diet plans may favour sustainable weight reduction. Furthermore, their use in diabetes management programmes may contribute to a better glycaemic control in patients, albeit with modest results. LNCS also provide dental health benefits when used in place of free sugars; (4) It is proposed that foods and beverages with LNCS could be included in dietary guidelines as alternative options to products sweetened with free sugars; (5) Continued education of health professionals is required, since they are a key source of information on issues related to food and health for both the general population and patients. With this in mind, the publication of position statements and consensus documents in the academic literature are extremely desirable.

A patient with myotonic dystrophy and associated primary hyperthyroidism and hyperparathyroidism is described; this association has not been reported previously, to the authors' knowledge. The patient also suffered from hypergonadotropic hypogonadism and hyperinsulinism with insulin resistance. The etiology of hyperthyroidism and hyperparathyroidism is not clear. At surgery, a parathyroid adenoma was extirpated, and a subtotal thyroidectomy was performed. Postoperative course was unremarkable, with consistently normal serum calcium levels but persistently elevated serum parathyroid hormone concentrations. The possibility that the patient had a residual hyperparathyroidism could not be eliminated. Thyroid function was normal. After surgery, the patient reported subjective improvement in his muscle strength. The authors conclude that both diseases-- hyperthyroidism and hyperparathyroidism--exert a negative effect on the myotonic dystrophy and that an early recognition of these two diseases is crucial for the favorable evolution of the patient.

Summary:We report on a case of ectopic Cushing's syndrome due to a thymic carcinoid tumour with periodic hormonogenesis. Periods of hormonal production averaged 27 days. Prior to bilateral adrenalectomy, mean (s.d) values of ACTH and cortisol were 202.1 (50.3) pg/ml and 46 (14.7) ug/dl, ACTH rising to 3996 ± 425 pg/ml (P < 0.01) and cortisol falling to 6.3 ± 1.5 jsg/dl (P < 0.01) in the immediate postoperative period. During the late postoperative period (2-13 months following surgery) ACTH levels fell to 509.3 (123.8) pg/ml (P < 0.01), but remaining even higher (P < 0.01) than before adrenalectomy. The pattern of ACTH in the present case suggests the existence of a negative feedback exerted by the cortisol over tumoral ACTH.

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