Hypoglycaemia after gastric bypass: mechanisms and treatment.

Hypoglycaemia after gastric bypass can be severe, but is uncommon, and is sometimes only revealed through monitoring glucose concentrations. The published literature is limited by the heterogeneity of the criteria used for diagnosis, arguing in favour of the Whipple triad with a glycaemia threshold of 55 mg/dl as the diagnostic reference. Women who lost most of their excess weight after gastric bypass, long after the surgery was performed, and who did not have diabetes before surgery are at the greatest risk. In this context, hypoglycaemia results from hyperinsulinism, which is either generated by pancreas anomalies (nesidioblastosis) and/or caused by an overstimulation of ß cells by incretins, mainly glucagon-like peptide-1 (GLP-1). Glucose absorption is both accelerated and increased because of the direct communication between the gastric pouch and the jejunum. This is a post-surgical exaggeration of a natural adaptation that is seen in patients who have not undergone surgery in whom glucose is infused directly into the jejunum. There is not always a correspondence between symptoms and biological traits; however, hyperinsulinism is constant if hypoglycaemia is severe and there are neuroglucopenic symptoms. The treatment relies firstly on changes in eating habits, splitting food intake into five to six daily meals, slowing gastric emptying, reducing the glycaemic load and glycaemic index of foods, using fructose and avoiding stress at meals. Pharmacological treatment with acarbose is efficient, but other drugs still need to be validated in a greater number of subjects (insulin, glucagon, calcium channel blockers, somatostatin analogues and GLP-1 analogues). Lastly, if the surgical option has to be used, the benefits (efficient symptom relief) and the risks (weight regain, diabetes) should be weighed carefully.

Determinants of changes in muscle mass after bariatric surgery.

AIM: The constituents of weight loss following bariatric surgery are poorly known. There is an expectation of a limited loss of lean body mass (LBM), and a significant loss of fat mass (FM) as well as muscle mass (MM), which could lead to functional loss and metabolic impairment. This prospective study analysed the determinants of MM changes after Roux-en-Y gastric bypass and sleeve gastrectomy. METHODS: The study cohort comprised 114 consecutive candidates for bariatric surgery referred to a bariatric surgery centre. Using DEXA, the subjects' body composition was assessed before, and three and 12 months (n=92) after, the surgery, along with their biological status. The main study outcome was changes in MM. RESULTS: At three months, patients had lost 20.3 kg, made up of 41% LBM and 59% FM. The contribution of MM to weight loss was 16.4%. Cluster analysis showed that 52 patients lost<15% of their weight as MM, while 62 patients lost>15% as MM. At 12 months, patients had lost 37 kg, made up of 70% FM and 30% LBM. At this time, only 27 patients lost>15% of their weight as MM. The determinants that were negatively and independently associated with MM changes at three months were FM loss and changes in glycaemia and thyroid-stimulating hormone ([TSH]; thyrotropin) before surgery, whereas change in glycaemia was the only 12-month determinant associated with MM changes. CONCLUSION: Two phenotypes - one with muscle wasting and the other with acceptable muscle loss - with a threshold of 15% and very few predictive factors were identified by this study.

[Large-vessel granulomatous vasculitis during the course of sarcoidosis: Takayasu's arteritis?]. / Angéite granulomateuse au cours d'une sarcoïdose : maladie de Takayasu ?

BACKGROUND: Vascular involvement in sarcoidosis is very rare and is characterized by preferential involvement of large vessels similar to that observed in Takayasu's disease. Distinguishing between these two diseases is often difficult and constitutes a diagnostic pitfall. The association between sarcoidosis and Takayasu's arteritis is not coincidental and a common physiopathological factor may exist; it suggests a possible aetiopathogenetic relationship between sarcoidosis and Takayasu's arteritis and casts doubt on whether this form of vasculitis is a disease in its own right or simply a syndrome caused by other diseases. CASE REPORT: We report the case of a man with a 10-year history of cutaneous and pulmonary sarcoidosis who developed ischaemia of the right upper limb evocative of Takayasu's arteritis. The patient was successfully treated with oral steroids and methotrexate. DISCUSSION: This case prompts discussion about the relationship between Takayasu's disease and sarcoidosis. Physicians should be aware of the possible occurrence of granulomatous arteritis during the course of sarcoidosis which requires a special work-up.

[What's new about microsatellite instability significance in human carcinogenesis?]. / Quoi de neuf sur la signification des instabilités microsatellitaires dans les pathologies tumorales humaines?

Microsatellite instabilities (MIN) represent a new type of mutation characterized by genomic instability (or replication error phenotype, RER+). First identified in sporadic and familial colorectal tumors, the RER+ phenotype has been sought in multiple types of cancers. Thus, two types of instability mechanisms have been shown: one due to inactivation of the mismatch repair system (phenotype RER+) and a second still unclear (instability of tri- and tetra-nucleotide repeats). In both cases, MIN seem to be the reflect of a new tumorigenesis pathway. In the context of mismatch repair defect, numerous observations show that, although instabilities seem to be random, they play a direct role in the tumoral process by altering genes that control cell growth and apoptosis. Today, MIN, as well as the detection of mutations in the DNA mismatch repair genes, can be used as diagnosis tools in oncology and provide usefull indications to adapt the chemotherapy to the disease.