An unusual cause of abdominal pain: spontaneous bilateral adrenal hemorrhage.

Bilateral adrenal hemorrhage (BAH) is a rare condition that can lead to acute adrenal insufficiency and death if not recognized and treated promptly. We report the case of a 30-year-old male who presented to the emergency department with acute abdominal pain, nausea, and vomiting. On emergency room admission, the first abdominal CT revealed normal adrenal glands without enlargement, but with the development of hypotension and hypoglycemia, a second CT performed four days later showed enlargement due to hemorrhage in both adrenals. The diagnosis of BAH associated with acute adrenal insufficiency was retained. Prompt treatment with intravenous and oral corticosteroids resulted in successful conservative management. We describe the clinical, biological, radiological and etiological features of this condition based on a review of the literature.

Clinical and biochemical characteristics and analysis of risk factors for euglycaemic diabetic ketoacidosis in type 2 diabetic individuals treated with SGLT2 inhibitors: A review of 72 cases over a 4.5-year period.

BACKGROUND AND AIMS: To study euglycemic diabetic ketoacidosis (euDKA) outcomes associated with sodium-glucose co-transporter 2 inhibitors (SGLT2is) METHODS: Review of 72 euDKA cases in T2DM between September 2015 and January 2020 (PUBMED). RESULTS: euDKA could occur at any time during SGLT2is treatment, with nausea, abdominal pain and vomiting as main symptoms. Hyperglycemia did not correlate with pH and ß-hydroxybutyrates. Low pH and high ß-hydroxybutyrates were significantly associated with euDKA. In biguanides users, acidosis was unrelated to lactic acidosis. euDKA occurred during fasting, surgery, acute infection, insulin deprivation (endogenous or exogenous). CONCLUSIONS: These data support avoidance of euDKA risk states in SGLT2i users.

[Diabetic euglycemic ketosis or ketoacidosis in individuals with type 2 diabetes treated by SGLT2 inhibitors: A series of Belgian clinical cases]. / Cétose ou acidocétose diabétique euglycémique chez des patients diabétiques de type 2 traités par inhibiteurs du SGLT2 : une série de cas cliniques en Belgique.

INTRODUCTION: Sodium-glucose cotransporter type 2 inhibitors (SGLT2i) are new therapeutic agents that improves the management of type 2 diabetes. Clinical trial results for SGLT2i have shown a reduction in blood glucose levels and a decrease in significant cardiovascular and renal complications related to diabetes. However, rare adverse events such as diabetic ketoacidosis have been reported in these clinical trials and in "real life". These ketoacidosis were atypical because the hyperglycemia was less severe than in traditional acute diabetes, hence the name of "euglycemic" ketoacidosis. We detail a series of local cases associated with the use of SGLT2i in type 2 diabetic patients. METHODS: This was a retrospective consecutive case study, with a review of medical records from 2016 to 2019. We identified 7 single episodes of "euglycemic" ketoacidosis associated with SGLT2i use in individuals with type 2 diabetes. RESULTS: Seven cases of type 2 diabetic individuals (M/F: 5/2) aged from 51 to 74years old were analysed. All had symptoms of hyperketonemia (fruity smelling breath, nausea or lack of appetite) and an increase level of capillary ß-hydroxybutyric acid despite a glycaemia between 112 and 280mg/dL. The risk factors for ketoacidosis identified in these patients were: prolonged fasting, infection, dehydration and significantly decreased in insulin secretory function (according to the HOMA model), revealing endogenous insulinopenia before ketoacidosis. CONCLUSION: The increasing use of SGLT2i in individuals with type 2 diabetes is likely to increase the number of ketoacidosis cases. It is essential to recognise this complication and prevent it according to each patient's risk factors.

Fibrosis of the thyroid gland caused by an IgG4-related sclerosing disease: three years of follow-up.

Immunoglobulin G4-related sclerosing disease (IgG4-RSD) represents a recently identified inflammatory disorder in which infiltration of IgG4 plasma cells causes fibrosis in organs. While IgG4-RSD is well documented in the pancreas and other organs, it is poorly characterized in the thyroid gland. We report a case of a 48-year-old female with a fibrotic thyroid mass associated with a retroperitoneal fibrosis. Diagnosed early as Riedel disease, the high serum IgG4, immunohistopathology and decreased fibrosis with corticosteroid therapy, finally confirm for the first time, the origin of IgG4-RSD fibrosis of the thyroid.

Assessing the incidence of gestational diabetes and neonatal outcomes using the IADPSG guidelines in comparison with the Carpenter and Coustan criteria in a Belgian general hospital.

We have conducted a systematic universal screening for gestational diabetes mellitus (GDM) since 2008, following the criteria outlined by the International Association of Diabetes and Pregnancy Study Group (IADPSG) since 2011. However, we recently replaced the IADPSG standards with those established by the Belgian French Language Gynecologists and Obstetricians Group (GGOLFB). These new criteria indicate GDM when fasting plasma glucose (FPG) is ≥0·92 g/l at the beginning of pregnancy or when an orally provoked hyperglycaemia test (75 g of glucose) between the twenty-fourth and twenty-eighth week results in an FPG of ≥0·92 g/l and/or ≥1·80 g/l after 1 hour and/or ≥1·53 g/l after 2 hours. The goal of this retrospective study was to evaluate the incidence of GDM, neonatal outcomes, and the use of insulin therapy 21 months post-implementation of the IADPSG criteria within our centre. A total of 393 patients were diagnosed with GDM from January 2009 to December 2012. After applying the new criteria, the incidence of GDM rose significantly from 8 to 23% (P<0·0001). However, there were no significant changes in the proportion of GDM patients requiring insulin therapy (34·2% versus 34·7%) or the rate of foetal large for gestational age (11·2% versus 8·8%). In addition, the ≥90% percentile decreased non-significantly from 96·3±0·6% to 94·3±0·70% (P = 0·057), whereas the lower quartiles and the proportion of cesarean deliveries (27·0% versus 25·6%) did not change significantly. Therefore, non-targeted screening significantly increased the incidence of GDM in our centre without significantly decreasing large for gestational age or the number of cesarean deliveries.

Prevalence and spectrum of SDHx mutations in pheochromocytoma and paraganglioma in patients from Belgium: an update.

Since the early 2000s, the prevalence and spectrum of mutations in genes encoding subunits of succinate dehydrogenase (SDHx) were reported in large cohorts of patients with pheochromocytoma (PC) and paraganglioma (PGL) from most Western countries. Unfortunately, in Belgium, no equivalent work was performed thus far. Therefore, the aim of the work was to look for mutations in SDHx genes and genotype-phenotype correlations in patients with PC and/or PGL from Belgium. Screening of the coding parts of SDHx genes and deletion search were performed in all patients with PC and/or PGL referred to the -Cliniques Universitaires Saint-Luc from 05/2003 to 05/2011. Genetic screening was performed in 59 unrelated head and neck (hn)PGLs (8 fami-lial) and 53 PCs (7 extra-adrenal; 3 metastatic). In hnPGLs, 10 different SDHD mutations (3 substitutions, 5 deletions, 2 splice site mutations) were detected in 16 patients, including 7 familial cases and 9 apparently sporadic cases. In the same subset, we found 8 different SDHB mutations (5 substitutions, 1 splice site mutation, 1 deletion, 1 duplication) in 10 patients with sporadic hnPGL without evidence of malignancy. No SDHx mutation was detected in patients harboring PCs and no SDHC mutation whatsoever. In conclusion, in our multicentric database of PC-PGLs from Belgium, (i) the prevalence of SDHx mutations was high in hnPGLs (44% in the whole subset, 37% of apparently sporadic cases); (ii) in sporadic cases, the prevalence of SDHB mutations was high (20%), similar to that of SDHD (18%); and (iii) no SDHx mutation was found in a subset of mostly adrenal, benign PCs.

Exenatide improves weight loss insulin sensitivity and ß-cell function following administration to a type 2 diabetic HIV patient on antiretroviral therapy.

The use of retroviral drugs in the treatment of infection by human immunodeficiency virus (HIV) is associated, especially for first generations, with side effects such as lipodystrophy, fatty liver and insulin resistance, which may trigger secondary diabetes or worsen existing diabetes. The use of Glucagon-Like Peptide-1 in obese patients with type 2 diabetes on HIV retroviral as an alternative to insulin therapy is not documented; we report the case of a 47-year-old treated with exenatide when insulin was discontinued. During the first year of treatment, exenatide, in combination with metformin and repaglinide, led to a weight loss of 14 kg and fat mass and waist circumference were respectively reduced from 31 to 25.5% and from 114 to 103 cm. Homeostatic model assessment (HOMA) was used to calculate ß-cell secretion which increased from 50 to 78% and insulin sensitivity which increased from 28 to 51%, reflecting a decrease in HbA(1c) by 1.9%. Exenatide may be a new therapeutic option for HIV-infected type 2 diabetes patients undergoing retroviral therapy.

One-year metabolic outcomes in patients with type 2 diabetes treated with exenatide in routine practice.

AIM: The study objective was to analyze, in everyday practice, the long-term metabolic effects of exenatide (for 9 and 12 months) in patients with type 2 diabetes not responding to treatments with metformin and sulphonylurea at maximum dosages. METHODS: A total of 299 type 2 diabetics were recruited from 14 centres specializing in diabetes care across Belgium. Main study endpoints were changes in HbA(1c), weight and waist circumference, and tolerability and compliance. Two patient cohorts were analyzed for effectiveness, with data available at 9 (n=90) and 12 (n=94) months of follow-up. RESULTS: Significant decreases in HbA(1c) of -1.3% and -1.6% were observed in the 9- and 12-month cohorts, respectively (P<0.001). The decrease in HbA(1c) was greater in patients with higher baseline levels (P<0.001), and the response was independent of baseline weight, body mass index (BMI), age, gender and diabetes duration. A progressive reduction of weight (4.9 kg) was also observed in the two cohorts at 9 and 12 months (P<0.001), with greater weight loss in patients with higher baseline BMI (P=0.046) and in female subjects (P=0.025). Waist circumference also decreased from baseline to endpoints. A correlation was observed between reduction in HbA(1c) and weight loss (P=0.019). Side effects, mainly of gastrointestinal origin, were reported in 33% (93/284 patients in the safety cohort). The rate of hypoglycaemia was 3.5%. Treatment was discontinued in 27% of patients (n=77) mainly due to drug inefficacy (53%, n=41) or adverse events (26%, n=20), or both (8%, n=6). CONCLUSION: Exenatide leads to long-term improvement of glycaemic control as well as weight loss in a majority of patients not responding to combined oral drug therapy in real-world clinical practice. However, no baseline factors predictive of response could be identified. Exenatide can be considered an effective treatment option in such patients, including those with high baseline HbA(1c) and long duration of diabetes.

Insulin sensitivity, adjusted beta-cell function and adiponectinaemia among lean drug-naive schizophrenic patients treated with atypical antipsychotic drugs: a nine-month prospective study.

Atypical antipsychotic drugs (AADs) induce weight gain and truncal adiposity, and even the metabolic syndrome (MetS), which may progress to IFG/IGT or DM. AAD effects in lean schizophrenic patients without MetS have not been documented, especially in terms of weight gain and changes in insulin sensitivity (S), beta-cell function (beta) and adiponectinaemia. We prospectively determined the effects of nine-month therapy with AADs on anthropometrics, metabolism and adiponectinaemia, including homoeostasis model assessment (HOMA) modelling of S, beta and betaxS (hyperbolic product, assessing individual beta adjusted for S). We analyzed 36 schizophrenic subjects (M/F: 24/12; Caucasian: n=23, North African: n=12, South Asian: n=1) aged 35+/- years (mean+/-one S.D.) free of MetS (NCEP-ATPIII), of whom 19 study completers were evaluated following AAD treatment. S, beta, betaxS and adiponectin were measured at zero, three and nine months. At nine months, BMI had risen from 22+/-2 to 25+/-2kg/m(2) (P<0.001) and waist circumference from 85+/-8 to 91+/-11cm (P<0.001), while adiponectin decreased from 10.4+/-5.1 to 7.4+/-3.8mug/mL (P<0.001). Blood pressure and lipids were unaffected. S decreased from 138+/-49 to 110+/-58% (P=0.006) and beta increased from 83+/-24 to 100+/-40% (P=0.034). As a result, betaxS decreased from 106+/-19 to 91+/-27% (P=0.015). Fasting glycaemia rose from 89+/-5 to 96+/-9mg/dL (P=0.007). On study completion, 21% had IFG. Long-term use of AADs in lean, drug-naive, schizophrenics initially free of MetS induced weight gain and truncal fat accumulation associated with decreases in adiponectin and hyperbolic product, explaining the increased fasting glycaemia and impaired fasting glucose seen in predisposed individuals.