Non-hodgkin’s lymphoma of the frontal sinus

Non-Hodgkin’s lymphoma (NHL) of the head and neck area is rare, and constitutes 0.4%–2% of all extranodal lymphomas and 6.4%–13% of extranodal lymphomas of the head and neck area^1–6. The maxillary antrum, nasal cavity and ethmoid sinus are the most common sites for this tumor³. Prognosis of the NHL affecting the paranasal sinuses and nasal cavity is poor with 33% of survival at 5 years^5–7. Failure of the treatment is local and with distant metastasis. Radiotherapy permits disease-free survival at 5 years in T1–T2 of 78% and in T3–T4 of 18%⁷. Only three cases in the literature have been described affecting the frontal sinus, in two cases there was infiltration of the other paranasal sinuses and in one case there was an isolated primary non-Hodgkin’s lymphoma of the frontal sinus^3,4 (Medline from 1966 to 2001). We present the second case reported in the literature of NHL exclusively affecting the frontal sinus showing local control 5 years after diagnosis.     

Type 2 diabetes mellitus, its treatment and risk for lymphoma

In this study, we have investigated a potential association between Type 2 diabetes mellitus and its treatment with the risk of lymphoma. Here, we report on 565 incident lymphoma (non-Hodgkin and Hodgkin), multiple myeloma, and chronic lymphocytic leukemia cases and 601 hospital controls in a Spanish multicentric case-control study. Information on diabetes mellitus diagnosis and treatment was obtained through personal interview together with information on other known or putative risk factors for lymphoma. The average age of the study population was 59 years. A medical diagnosis of diabetes was reported by 11% of the controls and 16.3% of cases. Patients with diabetes mellitus not treated with drugs were at an increased risk for lymphoma (OR=1.73, 95%CI=1.11, 2.68), and particularly for multiple myeloma (OR=2.80, 95%CI=1.40, 5.59). Patients treated with insulin had a non-significantly reduced risk for lymphoma (OR=0.70, 95%CI=0.29, 1.67). If replicated, this effect could be explained by a disappearance of hyperinsulinaemia in patients requiring insulin or to the continuous stimulation of the immune system by insulin.     

Simultaneous pancreas-kidney transplantation from donation after cardiac death: successful long-term outcomes

OBJECTIVE: The outcomes of simultaneous pancreas-kidney (SPK) transplantation with donor organs procured from donation after cardiac death (DCD) are compared with transplants performed with donor organs recovered from donation after brain death (DBD). SUMMARY BACKGROUND DATA: Concerns exist regarding the utilization of pancreata obtained from DCD donors. While it is known that DCD kidneys will have a higher rate of DGF, long-term functional graft survival data for DCD pancreata have not been reported. METHODS: A retrospective review of all DCD SPK transplants performed at a single center was undertaken. RESULTS: Patient, pancreas, and kidney survival at 5 years were similar between DCD and DBD organs. Pancreas function and outcomes were indistinguishable between the 2 modes of procurement. As expected, the DCD kidneys had an elevated rate of DGF, which had no significant long-term clinical impact. CONCLUSION: SPK transplantation using selected DCD donors is a safe and viable method to expand the organ pool for transplantation.     

Non-monomelic synchronous primary multicentric chondrosarcoma: a case report

We report a patient with simultaneous presentation of two histologically grade 2 conventional chondrosarcomas non-derived from pre-existing cartilaginous lesions, in the absence of pulmonary or visceral involvement. One tumour was located at the right proximal femur and the other one at the right scapula. There was no evidence of local recurrence or pulmonary or visceral involvement three years and a half after total scapulectomy and resection of the proximal third of the femur. To the best of our knowledge, this is the first report of a patient with two non-monomelic synchronous chondrosarcomas arising in two previously normal bones of the skeleton. Such cases are often difficult to differentiate from metastatic disease.     

Perinatal management of gastroschisis: analysis of a newly established clinical pathway

Purpose

The authors developed a clinical pathway for optimal management after antenatal diagnosis of gastroschisis. This is the outcomes analysis of our first 30 consecutive patients.

Method

Antenatal counseling was provided for all families with in-utero diagnosis of gastroschisis. Bowel dilatation, thickness, motility, amniotic fluid volume, and fetal development were followed by ultrasonography every 4 weeks. Babies were delivered by cesarean section between 36 and 38 weeks gestation if the lungs were mature or earlier for bowel complications. Gastroschisis repair was scheduled 90 minutes after birth. Primary repair was attempted in all through the abdominal wall defect without an additional incision, resulting in an umbilicus with no abdominal scar.

Results

Primary repair was achieved in 83%. Babies needed assisted ventilation for 3 days, reached full feeds by 19 days, and were discharged by 24 days (all medians). There were 3 (10%) deaths, all after staged repair.

Conclusions

Our new protocol of both scheduled elective cesarean section and early gastroschisis repair resulted in a higher proportion of primary repair, shorter duration of mechanical ventilation, earlier full feeds, and shorter length of stay. There was no increase in mortality or morbidity. The primary-repair babies had no mortality and had excellent cosmesis.     

The apolipoprotein E gene promoter (-219G/T) polymorphism determines insulin sensitivity in response to dietary fat in healthy young adults

Insulin sensitivity (IS) is determined by genetic and environmental factors, including diet. The apoE gene promoter -219G/T polymorphism is associated with coronary heart disease and increased postprandial triacylglycerol-rich lipoprotein concentration, circumstances related to insulin resistance. Thus, our aim was to determine whether this polymorphism modified the IS response to dietary fat in healthy young adults. Volunteers (n = 43) with the apoE3/E3 genotype (8 GG, 25 GT and 10 TT) completed 3 dietary periods, each lasting 4 wk. They first consumed a SFA-rich diet [38% fat (% of energy in the total diet), 20% SFA (% of energy in the total diet)], and then, in a randomized, crossover design, a carbohydrate (CHO)-rich diet (30% fat, 55% CHO) or a monounsaturated fatty acid (MUFA)-rich diet (38% fat, 22% MUFA). After each diet period, we investigated peripheral IS using the insulin suppression test. The steady-state plasma glucose (SSPG) concentration was lower (P < 0.05) in GG subjects than in GT and TT individuals, regardless of the diet consumed. Significant diet x genotype interactions were found for SSPG and plasma nonesterified FFA (NEFA) concentrations. Thus, the shift from the SFA-rich diet to the MUFA- or CHO-rich diets decreased (P < 0.05) the SSPG and NEFA concentrations in GG and GT, but not in TT subjects. In conclusion, carriers of the -219T allele are less insulin sensitive than GG individuals. Furthermore, only carriers of the -219G allele have improved IS when MUFA- or CHO-rich diets are consumed instead of a SFA-rich diet.     

Resistance to diet-induced obesity in mu-opioid receptor-deficient mice: evidence for a "thrifty gene"

Using pharmacological tools, a role for opioid receptors in the regulation of food intake has been documented. However, the involvement of specific receptor subtypes remains questionable, and little information is available regarding a role for opioid receptors in energy metabolism. Using adult male mice lacking the mu-opioid receptor (MOR) gene (MOR-/-), we show that the MOR is not essential for the maintenance of normal levels of ad libitum food intake but does modulate the efficiency of energy storage during high-fat diets through the regulation of energy partitioning. When fed a regular diet, MOR-/- mice displayed only subtle alterations in energy homeostasis, suggesting a relative overuse of fat as a fuel source in the fed state. When fed a high-fat diet, MOR-/- mice were resistant to obesity and impaired glucose tolerance, despite having similar energy intake to wild-type mice. This resistance to obesity was associated with a strong induction of the expression of key mitochondrial enzymes involved in fatty acid oxidation within skeletal muscle. This metabolic role of the MOR, which is consistent with the properties of a "thrifty gene," suggests that the MOR pathway is a potential target for pharmacological intervention in the treatment of obesity associated with the intake of fatty diets.