Sacral dural arteriovenous fistula: report of 4 cases

Spinal dural arteriovenous fistula (SDAVF) in the sacral region is relatively rare and remains difficult to diagnose because of the uncommon origin of its feeder. It also has higher incidence of recurrence than usual thoraco-lumbar lesion and needs subsequent treatment. We reviewed 51 cases of SDAVF over the past 10 years. Especially in patients with sacral lesion, clinical features and the findings on spinal angiography were analyzed. Four patients (7.8%) had SDAVF in the sacral region. In all cases, SDAVF were supplied by the lateral sacral artery. Multiple feeders were observed in 3 (75%) out of 4 patients and 2 patients (50%) had multiple fistulas. Endovascular embolizations were performed in all patients, and neurological symptoms were improved in two patients (50%) and the other two were stabilized (50%). There was no recurrence during a follow-up period of 3 months to 8 years. We should keep in mind that SDAVF in the sacral region can have multiple shunts and feeders derived from the lateral sacral artery.     

Frontofacial monobloc advancement using the Rigid External Distraction (RED-II) system

One-stage frontofacial monobloc advancement has been used to treat patients with craniofacial synostosis including Crouzon disease. Nishimoto et al. first applied a rigid external distraction system for two patients. However, precise surgical techniques and proper indication for this gradual distraction method have not yet been established. This report describes the advantages and detailed surgical methods of frontofacial monobloc advancement using a Rigid External Distraction (RED- II) System. Three patients with severe craniofacial synostosis including Crouzon disease and Treacher Collins syndrome were treated. The ages of patients were 9, 9, and 8 year old, respectively. The RED- II System was safely applied for these young children and cosmetic results were sufficient. No major postoperative complications occurred.     

Downregulation of ZnT8 expression in pancreatic β-cells of diabetic mice

Zinc transporter 8 (ZnT8) has been identified as a β-cell-specific Zinc transporter expressed in insulin-secretory granules. Recent genome wide association studies indicated that Arg325Trp polymorphism of Slc30a8 encoding ZnT8 is associated with susceptibility to type 2 diabetes. As a first step towards understanding the pathogenic role of ZnT8 in diabetes, we evaluated the expression of ZnT8 in mouse pancreas. A rabbit polyclonal antibody specific to ZnT8 was raised. The raised ZnT8 antibody reacted with mouse, rat and human ZnT8 expressed in β-cells without cross-reacting with other ZnTs. ZnT8 was expressed in α-, β- and PP-cells, but not in δ-cells, in adult mouse islets. During mouse pancreas development, ZnT8 expression was detected as early as embryonic day 15.5 when β-cells started to appear in large numbers. Finally, the expression level of ZnT8 was compared with pancreas of two diabetic model mice, db/db mice and Akita mice. In both animal models of diabetes, ZnT8 expression was remarkably downregulated in the early stage of diabetes. As a conclusion, ZnT8 is expressed in multiple lineages of endocrine cells in the pancreas. Our findings suggest that downregulation of ZnT8 may be associated with impaired function of β-cells in diabetes.     

High risks of all-cause and cardiovascular deaths in apparently healthy middle-aged people with preserved glomerular filtration rate and albuminuria: A prospective cohort study

Background

The reason why coexistence of preserved estimated glomerular filtration rate (eGFR) and albuminuria contributes to a high risk of death and which cause of death increases all-cause mortality have not been elucidated.

Methods

A total of 16,759 participants aged 40 to 69 years with normal or mildly reduced eGFR (45–119 ml/min/1.73 m²) were enrolled and divided into six groups (group 1, eGFR: 90–119 without albuminuria; group 2, eGFR: 90–119 with albuminuria; group 3, eGFR: 60–89 without albuminuria (reference); group 4, eGFR: 60–89 with albuminuria; group 5, eGFR: 45–59 without albuminuria; group 6, eGFR: 45–59 with albuminuria) based on GFR estimated by using the CKD-EPI study equation modified by a Japanese coefficient and albuminuria (urine albumin–creatinine ratio ≥ 30 mg/g). Outcomes included all-cause death (ACD), cardiovascular death (CVD) and neoplasm-related death (NPD). Multivariable-adjusted mortality rate ratios (RR) and their 95% confidence intervals (CIs) in the groups were estimated by Poisson's regression analysis.

Results

The highest risk of ACD (RR (95% CIs): 3.95 (2.08–7.52)), CVD (7.15 (2.25–22.7)) and NPB (3.25 (1.26–8.38)) was observed in group 2. Subjects in group 2 were relatively young and had the highest levels of body mass index, blood pressure and HbA_1c and the highest prevalence of diabetes and metabolic syndrome.

Conclusion

Coexistence of preserved eGFR and albuminuria increases risks for ACD, CVD and NPD. Relatively young metabolic persons having both preserved eGFR and albuminuria should be considered as a very high-risk population.     

Therapeutic effect of ARBs on insulin resistance and liver injury in patients with NAFLD and chronic hepatitis C: a pilot study

Fatty liver is one of the local morphological manifestations of metabolic syndrome and is frequently associated with insulin resistance. Insulin resistance is also common in patients with chronic hepatitis C. Hyperinsulinemia is an independent risk factor for hypertension and cardiovascular mortality. The aim of this study was to evaluate the therapeutic efficacy of angiotensin II receptor blockers (ARBs), telmisartan and olmesartan, for patients with non-alcoholic fatty liver disease (NAFLD) and chronic hepatitis C (CH-C). We analyzed the incidence of obesity, insulin resistance, and other disorders in patients with NAFLD (Group A), CH-C (Group B), or other liver diseases (Group C). We evaluated whether the ARBs, telmisartan and olmesartan, improved insulin resistance and liver injury by measuring the homeostasis model assessment ratio of insulin resistance (HOMA-IR) and serum alanine aminotransferase (ALT). The incidence of obesity (BMI >/=25 kg/m2) was significantly higher in Group A than in Groups B and C. The incidence of insulin resistance (HOMA-IR >/=2.5) in Groups A and B was significantly higher than in Group C. Regular doses of telmisartan and olmesartan significantly improved HOMA-IR and ALT levels not only in NAFLD patients but also in patients with CH-C. The effects tended to be more notable with telmisartan. In conclusion, telmisartan and olmesartan improved insulin sensitivity and may possibly be used as liver protecting agents in CH-C as well as NAFLD patients.