Long-term Outcome with the Prophylactic Use of Polypropylene Mesh in Morbidly Obese Patients Undergoing Biliopancreatic Diversion

The use of prosthetic material to prevent incisional hernia in clean-contaminated procedures as bariatric surgery remains controversial. We present our experience on 45 consecutive morbidly obese patients undergoing biliopancreatic diversion that was closed using a polypropylene mesh. Moreover, we reviewed the outcome of the 50 previous consecutive obese patients who underwent biliopancreatic diversion and conventional closure of the abdomen in order to compare the outcome between the two groups after a minimum follow-up of 2 years. Between January 2006 and February 2010, 95 morbidly obese patients underwent open biliopancreatic diversion at our department. During the first 2 years of our experience, there were 50 obese patients whose open biliopancreatic diversion was closed conventionally (without mesh). Starting on February 2008 and until February 2010, 45 patients received prophylactic midline reinforcement by the positioning of retrorectal muscle polypropylene mesh. The outcome at 3, 6, 12, and 24 months was analyzed comparing the two groups of patients. No mesh infection occurred. Minor local complications occurred similarly in both groups. The incidence of postoperative hernia was significantly higher in the group conventionally closed (30%) than in the mesh group (4.4%) at 2-year follow-up (p < 0.05). The prophylactic use of mesh in open bariatric surgery is safe and effective at 2-year follow-up.     

Lidocaine toxicity secondary to local anesthesia administered in the community for elective circumcision

We report three previously healthy infants aged, respectively, 23 days, 6 weeks, and 3 months with systemic lidocaine toxicity following administration of subcutaneous lidocaine for regional anesthesia during an elective circumcision. The patients developed a generalized seizure requiring endotracheal intubation but recovered fully with supportive care. We report the clinical details of these cases as well as a review of lidocaine toxicity.     

Docetaxel in combination with carboplatin for the treatment of advanced non-small cell lung carcinoma: a multicentre phase I study

Docetaxel and carboplatin have shown in vitro and in vivo activity against non-small cell lung cancer (NSCLC). A phase I study was conducted in order to determine the dose-limiting toxicities (DLTs) and the maximum tolerated doses (MTDs) of their combination. Chemotherapy-na?ve patients with stage IIIB and IV NSCLC, age<75 years old, performance status (WHO) 0-2, with adequate bone marrow, renal, liver and cardiac function, were treated with docetaxel and carboplatin. Docetaxel was given at escalated doses starting from 70 mg/m(2) with increments of 10 mg/m(2) followed by carboplatin also administered at escalated doses starting from AUC 5 to 7 AUC (mg/ml. min); the regimen was administered every 3 weeks. No colony-stimulating factor or intrapatient escalation was allowed. The toxicity of the regimen was assessed during the first chemotherapy cycle. 35 enrolled patients received a total of 114 chemotherapy cycles (median 3 cycles/patient; range: 1-8). All patients were assessable for toxicity. Neutropenia was the main dose-limiting toxicity of the regimen; overall, grade 3/4 neutropenia occurred in 16 (14%) cycles; six (5%) neutropenic episodes were complicated with fever but there was no septic death. Grade 3/4 thrombocytopenia was uncommon (two cycles; 2%). Grade 3/4 diarrhoea occurred in 5 (14%) patients whilst neurotoxicity, fatigue and mucositis were extremely uncommon. Two MTDs were defined: the MTD(1) was docetaxel 80 mg/m(2) and carboplatin AUC 7 mg/ml x min whilst MTD(2) was docetaxel 100 mg/m(2) and carboplatin AUC 6 mg/ml x min. The combination of docetaxel and carboplatin is a feasible and well-tolerated outpatient regimen for the treatment of patients with locally advanced and metastatic NSCLC. This regimen merits further investigation in phase II trials.     

Three independent mutations in the TSC2 gene in a family with tuberous sclerosis

Tuberous sclerosis complex (TSC) is a rare autosomal dominant disorder characterized by hamartomas and hamartias in multiple organs. TSC is caused by a wide spectrum of mutations within the TSC1 and TSC2 genes. Here, we report a unique family with three independent pathological mutations in TSC2. A c.1322G>A mutation in exon 12 created a stop codon, whereas a second mutation in exon 23 (c.2713C>T) was a missense change. The third mutation was a 4 base pair deletion in intron 20 of TSC2. We showed that this mutation was responsible for abnormal splicing. The three mutations were most likely de novo, as parents of affected patients did not present any features of TSC. In addition, we showed gonadal mosaicism in a branch of the family. To our knowledge, several independent mutations in TSC2 have never been observed in a single family. The probability of finding a family with three different pathological TSC2 mutations is extremely low. We discuss two main hypotheses that may be raised to explain this recurrence: (i) the TSC2 mutation rate is underestimated. In such a case, the likelihood of finding a family with three independent mutations in TSC2 may not be dramatically low; (ii) a heritable defect in a DNA repair gene (eg, mismatch repair gene) segregating in the family that is unlinked to the TSC2 gene might predispose to the occurrence of multiple TSC2 gene mutations, used as a specific target during embryogenesis.