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Bernd Schultes, Barbara Ernst, Florian Schmid and Martin Thurnheer

Context

Obesity resulting from damage to the hypothalamus, i.e. hypothalamic obesity, is a severe condition that currently lacks any effective evidence-based therapy.

Objective

Our goal was to describe the course of hypothalamic obesity in a craniopharyngioma patient treated with distal gastric bypass surgery and to outline distinct aspects of multidisciplinary case management.

Patient and methods

A 29-year-old man, who had undergone craniopharyngioma resection at the age of 8, was referred to our Interdisciplinary Obesity Centre with a body mass index (BMI) of 52.0 kg/m2, type 2 diabetes and obstructive sleep apnoea syndrome (OSAS). After careful preoperative preparation, including the adjustment of hormone substitution therapy for panhypopituitarism, nutritional counselling and a supervised exercise program, he underwent a distal gastric bypass operation.

Results

Eighteen months after the operation the patient's BMI had decreased to 31.9 kg/m2, type 2 diabetes was in complete remission, and OSAS appeared to be improved. Also, feelings of hunger were markedly reduced after the operation. A standard regimen of supplements successfully prevented any severe nutritional deficiencies. After weight loss, the dose of hydrocortisone could be distinctly reduced without any signs of adrenal insufficiency while GH substitution had to be markedly increased to achieve normal IGF1 levels.

Conclusions

Our case demonstrates that within a multidisciplinary team approach, a distal gastric bypass operation can be a safe and highly effective therapy for patients with hypothalamic obesity. Also, our findings hint at an effect of gastric bypass surgery on hunger and eating behaviour that may not essentially rely on hypothalamic mechanisms.

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Kerstin M Oltmanns, Baerbel Dodt, Bernd Schultes, Hans H Raspe, Ulrich Schweiger, Jan Born, Horst L Fehm and Achim Peters

Objective: The prevalence of type 2 diabetes mellitus is increasing rapidly in industrialized countries, and adrenal glucocorticoids may intensify this disease. We sought to assess the relationship between diabetes-associated metabolic disturbances and cortisol concentrations in patients with type 2 diabetes.

Design: We investigated 190 type 2 diabetic patients who volunteered from a population study of 12 430 people in Luebeck and its suburbs. The target population comprised men and women born between 1939 and 1958 who initially received a postal questionnaire about their health status. We identified 346 subjects with confirmed diabetes mellitus and 216 patients participated in the study. Patients with type 1 diabetes were excluded.

Methods: Five salivary cortisol samples were collected before and after lunch, in the evening and then the next morning before and after standing. Clinical variables associated with diabetes were measured and correlated with cortisol concentrations.

Results: None of the cohort had salivary cortisol concentrations that exceeded the normally accepted range. Based on cortisol samples collected just prior to a standard lunch, the cohort was divided into tertiles. Cortisol was positively related to: fasting blood, urinary and postprandial glucose; glycosylated hemoglobin; and systolic and diastolic blood pressures (all P < 0.05). Cortisol concentrations also correlated with the relative abdominal mass (P < 0.05) when patients with marked glucosuria were excluded.

Conclusions: The degree of severity of several clinical measures of type 2 diabetes correlates with cortisol concentrations. Moreover, the results provide evidence for a positive relationship between metabolic disturbances and cortisol concentrations that are within the accepted normal range.