Conversion to hypertrophic vertebral pseudarthrosis following percutaneous vertebroplasty

To determine the role of percutaneous vertebroplasty (PVP) in bone formation and the union of vertebral pseudarthrosis, we analyzed 14 patients with an average follow-up duration of 21 months. Evaluation methods included back pain (visual analog scale: VAS), wedge angle, dynamic mobility, radiographic remodeling including callus and spur formation, and union status. The Student's t test was used for statistical analysis and a probability of less than 0.05 was determined as a significant difference. Back pain improved in all 14 patients with a VAS score of 57.8 ± 23.5 mm (average ± standard deviation) preoperatively and 14.7 ± 16.4 mm at the final follow-up (P < 0.001). The wedge angle decreased from 21.6° ± 8.3° (average ± standard deviation) preoperatively to 13.2° ± 6.9° at the final follow-up (P < 0.001). Callus formation was seen in four patients. Bony spurs were seen in the affected vertebra in preoperative radiographs in all patients, and were further developed to a solidified form during follow up after PVP. Dynamic mobility of the affected vertebrae was 6.9 ± 2.9 mm preoperatively, which decreased to 1.1° ± 0.7° at the final follow-up (P < 0.001). Notably, all patients showed the dynamic vertebral mobility of 2 mm or less. Nevertheless, only two patients exhibited the dynamic vertebral mobility of 0 mm at the final follow-up, which is referred to as bone union. These findings indicate that PVP serves as a mechanical stabilizer for vertebral pseudarthrosis, which leads to immediate pain relief and segmental bony responses.     

Vascular-Resident CD169-Positive Monocytes and Macrophages Control Neutrophil Accumulation in the Kidney with Ischemia-Reperfusion Injury

Monocytes and kidney-resident macrophages are considered to be involved in the pathogenesis of renal ischemia-reperfusion injury (IRI). Several subsets of monocytes and macrophages are localized in the injured tissue, but the pathologic roles of these cells are not fully understood. Here, we show that CD169⁺ monocytes and macrophages have a critical role in preventing excessive inflammation in IRI by downregulating intercellular adhesion molecule-1 (ICAM-1) expression on vascular endothelial cells. Mice depleted of CD169⁺ cells showed enhanced endothelial ICAM-1 expression and developed irreversible renal damage associated with infiltration of a large number of neutrophils. The perivascular localization of CD169⁺ monocytes and macrophages indicated direct interaction with blood vessels, and coculture experiments showed that the direct interaction of CD169⁺ cell-depleted peripheral blood leukocytes augments the expression levels of ICAM-1 on endothelial cells. Notably, the transfer of Ly6C^lo monocytes into CD169⁺ cell-depleted mice rescued the mice from lethal renal injury and normalized renal ICAM-1 expression levels, indicating that the Ly6C^lo subset of CD169⁺ monocytes has a major role in the regulation of inflammation. Our findings highlight the previously unknown role of CD169⁺ monocytes and macrophages in the maintenance of vascular homeostasis and provide new approaches to the treatment of renal IRI.     

Anti-pruritic effect of nemolizumab in hemodialysis patients with uremic pruritus: a phase II,randomized, double-blind,placebo-controlled clinical study

Clinical and Experimental Nephrology - The pathophysiology of uremic pruritus (UP), which is characterized by systemic and intractable itching, remains unclear. As interleukin (IL)-31 may be...     

Activation of vascular protein kinase C-beta inhibits Akt-dependent endothelial nitric oxide synthase function in obesity-associated insulin resistance

Activation of protein kinase C (PKC) in vascular tissue is associated with endothelial dysfunction and insulin resistance. However, the effect of vascular PKC activation on insulin-stimulated endothelial nitric oxide (NO) synthase (eNOS) regulation has not been characterized in obesity-associated insulin resistance. Diacylglycerol (DAG) concentration and PKC activity were increased in the aorta of Zucker fatty compared with Zucker lean rats. Insulin-stimulated increases in Akt phosphorylation and cGMP concentration (a measure of NO bioavailability) after euglycemic-hyperinsulinemic clamp were blunted in the aorta of fatty compared with lean rats but were partly normalized after 2 weeks of treatment with the PKCbeta inhibitor ruboxistaurin (LY333531). In endothelial cell culture, overexpression of PKCbeta1 and -beta2, but not PKCalpha, -delta, or -zeta, decreased insulin-stimulated Akt phosphorylation and eNOS expression. Overexpression of PKCbeta1 and -beta2, but not PKCalpha or -delta, also decreased Akt phosphorylation stimulated by vascular endothelial growth factor (VEGF). In microvessels isolated from transgenic mice overexpressing PKCbeta2 only in vascular cells, Akt phosphorylation stimulated by insulin was decreased compared with wild-type mice. Thus, activation of PKCbeta in endothelial cells and vascular tissue inhibits Akt activation by insulin and VEGF, inhibits Akt-dependent eNOS regulation by insulin, and causes endothelial dysfunction in obesity-associated insulin resistance.     

Prevalence of deep venous thrombosis in the lower limbs and the pelvis and pulmonary embolism in patients with positive antiphospholipid antibodies

BACKGROUND: Antiphospholipid antibodies (AA) are immunoglobulins that cross-react with phospholipid on cell membrane, and are therefore associated with a hypercoagulable state manifested by arterial/venous thromboses. We aimed to determine the prevalence of deep venous thrombosis in the lower limbs and the pelvic region (DVT) and pulmonary embolism (PE) in patients with positive AA. METHODS: Sixty-six patients (48 female, 18 male) with positive lupus anticoagulant (LA) and/or positive anticardiolipin antibody (aCL) underwent radionuclide (RN) venography with 370 MBq of 99mTc-MAA. Pulmonary perfusion scintigraphy was performed in 58 patients. Fifteen patients had positive LA and positive aCL (LA+/aCL+), 33 patients had positive LA only (LA+/ aCL-) and 18 patients had positive aCL only (LA-/aCL+). 43 patients were diagnosed with primary antiphospholipid syndrome (APS) and 19 were diagnosed with APS associated with SLE. RESULTS: DVT was detected in 21 of 66 patients (32%). Patients with LA+/aCL+ showed higher prevalence of DVT (53%) as compared to LA+/aCL- (27%) and LA-/aCL+ (22%). PE was found in 13 of 58 patients (22%). The prevalence of PE was higher in patients with positive aCL (33% in LA+/aCL+; 36% in LA-/aCL+) than in patients with negative aCL (10%). CONCLUSION: Because of the high prevalence of DVT and PE in patients with AA, RN scintigraphy must be recommended in screening for these clinical troubles. These results indicate that the prevalence of DVT and PE may vary in subgroups of AA.     

High concentration sevoflurane induction of anesthesia accelerates onset of vecuronium neuromuscular blockade

PURPOSE: To investigate neuromuscular block using accelography after administration of vecuronium under sevoflurane 8% induction and maintenance with sevoflurane 2% in adults. METHODS: Patients were allocated to three groups: (1) group I: anesthesia was induced and maintained with propofol and fentanyl (n= 15), (2) group II: anesthesia was induced with propofol and maintained with N2O(66%)-O2-sevoflurane 2% (n = 15), (3) group III: anesthesia was induced with sevoflurane 8% using a vital capacity inhalation induction and maintained with N2O(66%)-O2-sevoflurane 2% (n = 15). 0.1 mg x kg(-1) vecuronium was used for paralysis three minutes after anesthetic induction and reversed using intravenous 0.04 mg x kg(-1) neostigmine with 0.02 mg kg atropine when the train-of-four (TOF) ratio returned to 25%. RESULTS: The onset time from initial administration of vecuronium to maximal block in the group III was shorter than that in the groups I and II (139 +/- 35, 193 +/- 35 and 188 +/- 47s, respectively: P < 0.05). The clinical duration from maximal block to 25% recovery of TOF ratio in group II and III was longer than that in the group I (47 +/- 15, 48 +/- 14 and 36 +/- 10 min, respectively: P < 0.05). The reversal times from administration of neostigmine to 75% of TOF ratio in groups II and III were longer than that in the group I (196 +/- 53, 208 +/- 64 and 136 +/- 28s, respectively: P < 0.05). CONCLUSIONS: Vital capacity inhalation induction of anesthesia with sevoflurane accelerates onset and prolongs duration of vecuronium neuromuscular block compared with propofol-fentanyl anesthesia.     

Prolonged hoarseness and arytenoid dislocation after endotracheal intubation

We present a case of prolonged hoarseness after tracheal intubation in a 62-year-old woman with bronchial asthma who underwent a pylorogastrectomy under a combination of epidural and general anesthesia. After the induction of anesthesia, the patient was carefully intubated using a 7.5-mm cuffed endotracheal tube without a stylet to avoid causing an asthma attack; the patient was extubated approximately 6 hours after the tracheal intubation. On the first postoperative day, the patient complained of hoarseness, vocal fatigue, and dysphagia. A direct laryngoscopy performed by an otorhinolaryngologist revealed dyskinesia of the left vocal cord and sufficient arytenoid cartilage mobility. The poor vocal fold mobility was probably caused by the force exerted on the left arytenoid by the convex curvature of the endotracheal tube, which had been inserted from the right side of the mouth, or a backward pressure on the thyroid cartilage during intubation. Early treatment is crucial in such cases, since the cricoarytenoid joint can become fibrosed in an unfavorable position. Fortunately, all the symptoms disappeared after one month in the present case. Although the trigger responsible for the spontaneous healing remains unknown, natural recovery might be associated with proper use of the vocal cords.     

Analysis of Mutations in the Urate Transporter 1 (URAT1) Gene of Japanese Patients with Hypouricemia in Northern Japan and Review of the Literature

Background. Renal hypouricemia is an autosomal recessive disorder resulting from inactivating mutations in the urate transporter 1 (URAT1) encoded by SLC22A12. To date, 10 mutations have been identified and W258X in the URAT1 gene is the predominant cause in middle to southwestern Japan. However, it is still unclear whether there is a regional specific distribution of mutations in northern Japan. In this study, we analyzed mutations in the URAT1 gene of five Japanese patients with renal hypouricemia in northern Japan. Methods. Peripheral blood mononuclear cells were isolated from patients with hypouricemia and healthy control subjects. A mutation analysis of the URAT1 gene was performed completely by direct automated sequencing of polymerase chain reaction-amplified DNA products. Results. We identified two mutations. These mutations [c.269G>A (R90H) and c.774G>A (W258X)] have been reported in Japanese patients. Two of five patients were homozygotes (W258X), two carried single heterozygous mutations (W258X), and the remaining one was a compound heterozygote (R90H and W258X). Conclusions. Our study suggests that there is no regional different distribution of the URAT1 genetic mutations in Japanese with renal hypouricemia.