Endocrine Abstracts

Introduction: Inadequate glucocorticoid replacement therapy in Addison disease leads to an increased risk of both cardiovascular disease and metabolic syndrome. The metabolic effects of long-life corticosteroid exposure are due to physiological mechanisms that are associated with carbohydrate metabolism disorder, dyslipidemia and insulin resistance. In this study, we aimed to determine the prevalence and predictive factors of metabolic syndrome in patients with Addison disease.

Patients and methods: A cross sectional study performed between March 2020 and July 2021, including 50 patients with Addison disease. Metabolic syndrome was assessed by referring to the National Cholesterol Education Program-Adult Treatment Panel III.

Results: Mean age was 49.5±13.9 years (40 females versus 10 males). Average duration of the disease was 13.9±8.7 years (5–35 years). All patients were on hydrocortisone replacement, taking daily 27.4±6.7 mg (15–42.1 mg). The average weight was 72.5 kg (62–107 kg).Progressive weight gain was observed in 70% of patients. This gain was more pronounced during the first year of follow-up and estimated at 7.4 kg on average. Mean Body Mass Index (BMI) was 28.1 kg/m² (21,2–45,8 kg/m²).Twenty four (48%) patients were obese. Mean waist circumference was 107±11.8 cm (65–121 cm) for woman and 105.1±9.6 cm (64–119 cm) for men. Android fat distribution was found in 60% of patients versus 12% at time of diagnosis. Glucose intolerance was found in over a third of patients (38%).Among those patients, 31,6% had type 2 diabetes. Hypertriglyceridemia was found in 2 patients. Five patients had low HDL-cholesterol level. Metabolic syndrome was found in 24% of patients versus only one patient at time of diagnosis. No significant correlation was identified between Addison disease duration and the occurrence of metabolic syndrome. Daily hydrocortisone dose was significantly higher among patients having metabolic syndrome (P=0.04).As well, cumulative hydrocortisone dose was higher among those patients but without significant difference (P=0.5).

Conclusion: Similarly, to anti-inflammatory corticotherapy, a broad range of metabolic effects including insulin resistance and profound alterations in carbohydrate and lipid metabolism impedes glucocorticoid replacement therapy.