Endoscopic full-thickness resection of a lateral spreading rectal tumor after unplanned injection of dilute hyaluronic acid into the subserosal layer (with video)

A 74-year-old woman underwent colonoscopy for investigation of a liver tumor. A lateral spreading tumor of the non-granular type (LST-NG), 25?mm in diameter, was detected at the rectosigmoid junction. As magnifying image-enhanced colonoscopy suggested a tubulovillous adenoma, endoscopic mucosal resection (EMR) was chosen for removal of the LST-NG. The lesion was effectively and evenly lifted after injection of 0.4% hyaluronic acid diluted with glycerol in the ratio of 1:1. A small amount of indigo-carmine dye was also added for coloration of the plane of resection. The lesion was completely removed en bloc. Although a blue-colored layer was identified in the resection defect, a small amount of a whitish layer was detected above the blue layer. The muscle layer was clearly located on the underside of the resected polyp. A total of 14 endoclips were used to close the defect completely. The patient was successfully treated conservatively without surgery. Histology of the resected specimen showed that it contained a tubulovillous adenoma with the submucosal layer and both layers of the muscularis propria. The surgical margin was free of neoplastic change horizontally and vertically. To the best of our knowledge, this is the first case report of full-thickness resection associated with EMR after unplanned injection of dilute hyaluronic acid into the subserosal layer rather than the intended submucosal layer. We describe how to promptly recognize this complication during colonoscopy, in order to achieve immediate closure of the defect, with the identification of a "mirror target sign" on the colonic wall.     

Estimation of salt intake from spot urine samples in patients with chronic kidney disease

ABSTRACT: BACKGROUND: High salt intake in patients with chronic kidney disease (CKD) may cause high blood pressure and increased albuminuria. Although, the estimation of salt intake is essential, there are no easy methods to estimate real salt intake. METHODS: Salt intake was assessed by determining urinary sodium excretion from the collected urine samples. Estimation of salt intake by spot urine was calculated by Tanaka's formula. The correlation between estimated and measured sodium excretion was evaluated by Pearson's correlation coefficients. Performance of equation was estimated by median bias, interquartile range (IQR), proportion of estimates within 30 % deviation of measured sodium excretion (P30) and root mean square error (RMSE).The sensitivity and specificity of estimated against measured sodium excretion were separately assessed by receiver-operating characteristic (ROC) curves. RESULTS: A total of 334 urine samples from 96 patients were examined. Mean age was 58 +/- 16 years, and estimated glomerular filtration rate (eGFR) was 53 +/- 27 mL/min. Among these patients, 35 had CKD stage 1 or 2, 39 had stage 3, and 22 had stage 4 or 5. Estimated sodium excretion significantly correlated with measured sodium excretion (R = 0.52, P < 0.01). There was apparent correlation in patients with eGFR <30 mL/min (R = 0.60, P < 0.01). Moreover, IQR was lower and P30 was higher in patients with eGFR < 30 mL/min. Estimated sodium excretion had high accuracy to predict measured sodium excretion, especially when the cutoff point was >170 mEq/day (AUC 0.835). CONCLUSIONS: The present study demonstrated that spot urine can be used to estimate sodium excretion, especially in patients with low eGFR.     

Impact of glutathione S-transferase T1 gene polymorphisms on acute cellular rejection in living donor liver transplantation

It has previously been demonstrated that glutathione S-transferase T1 (GSTT1) genetic mismatch between recipient and donor is a risk factor for developing immune-mediated hepatitis following liver transplantation and for antibody-mediated rejection in renal transplantation. Little is known whether the GSTT1 gene polymorphism affects the incidence of acute cellular rejection (ACR) following living donor liver transplantation (LDLT). Patients underwent LDLT at Nagoya University or Kyoto University, Japan, between 2004 and 2009. Genotyping of GSTT1 genes (null or present genotype) was conducted in recipients and donors. A total of 155 LDLT cases were examined. Forty-seven recipients (30.3%) developed early ACR. There was no association of recipient GSTT1 genotype with ACR incidence. However, ACR incidence was significantly higher in recipients transplanted from GSTT1 present genotype donors than in those transplanted from GSTT1 null genotype donors [odds ratio (OR) = 2.64, 95% confidence interval (CI) = 1.12–5.83, p = 0.016]. Moreover, GSTT1 recipient/donor genotype mismatch (present/null or null/present) was significantly associated with ACR development (OR = 2.28, 95% CI = 1.12–4.61, p = 0.022). The genotyping of GSTT1 in recipients and donors might be useful to stratify the liver transplant recipients according to risk of ACR.     

Atypical Pneumocystis jiroveci pneumonia with multiple nodular granulomas after rituximab for refractory nephrotic syndrome

Background

Rituximab, an anti-CD20 antibody that targets B cells, is a promising agent against steroid-dependent and steroid-resistant nephrotic syndrome in children.

Case-Diagnosis/Treatment

We report a 3-year-old boy who presented with atypical Pneumocystis jiroveci pneumonia (PCP) following administration of rituximab for refractory nephrotic syndrome. He had received cyclosporine and daily prednisolone for over 1?year. Following rituximab therapy, a hazy shadow was observed on his chest X-ray. Chest-computed tomography revealed multiple nodular lesions in bilateral lungs, although his clinical symptoms were subtle. PCR analysis demonstrated the presence of Pneumocystis DNA in his bronchoalveolar lavage. Lung wedge resection of the nodular lesion exhibited granulomas containing a few cysts of P. jiroveci that primarily consisted of T cells and histiocytes and lacked B cells. A deficiency of B cells following rituximab treatment suggests a dramatic effect on the immune response and, therefore, could result in granulomatous PCP. Nodular granulomatous lesions of PCP comprise an emerging concept previously reported in adults with hematological disease, bone marrow transplant, or treatment with rituximab. We report the first pediatric case of nodular PCP. Granulomatous PCP can be life-threatening. Moreover, bronchoalveolar lavage often fails to demonstrate the presence of P. jiroveci DNA. Wedge biopsy is warranted for definitive diagnosis. Our patient fully recovered with sulfamethoxazole/trimethoprim treatment because of early detection.

Conclusions

The indication of rituximab for refractory nephrotic syndrome has increased recently. Therefore, recognition of the risk of atypical PCP is important. Our findings suggest that PCP prophylaxis should be considered following rituximab therapy.     

CARPAL TUNNEL SYNDROME IN PATIENTS ON LONG-TERM HAEMODIALYSIS

The purpose of this study was to describe the pathophysiology of carpal tunnel syndrome (CTS) in patients on long-term haemodialysis. We examined 110 patients, who had been having haemodialysis for chronic renal failure and had CTS, to clarify the clinical features and electrophysiological changes in peripheral nerves. There was a significant correlation between the incidence of CTS and the duration of haemodialysis. Compared with idiopathic CTS, CTS caused by long-term haemodialysis had relatively limited postoperative improvement. Symptoms recurred postoperatively in 11 patients (19%) of those with CTS caused by long-term haemodialysis. Electrophysiological measurements of sensory nerve conduction velocity showed that it was slower in distal segments of the median nerve in patients on haemodialysis compared with normal volunteers. Nerve conduction velocity in the carpal tunnel was significantly delayed (p &lt; 0.05) in the patients with CTS on long-term haemodialysis. N_9-13 interpeak latencies were significantly longer (p &lt; 0.05) in subjects who had had haemodialysis for at least 10 years. All the patients with advanced destructive spondyloarthropathy had longer N_9-13 interpeak latency. These results suggest that CTS in patients on long-term haemodialysis has its basis in neuropathy. The clinical course of CTS in these patients is different from that of patients with idiopathic CTS, because the neuropathy involves not only the carpal tunnel region, but also the proximal part of the median nerve both diffusely and progressively.     

A practical prediction model for early hematoma expansion in spontaneous deep ganglionic intracerebral hemorrhage

Objective

Early hematoma expansion is a known cause of morbidity and mortality in patients with intracerebral hemorrhage (ICH). The goal of this study was to identify clinical predictors of ICH growth in the acute stage.

Materials and methods

We studied 201 patients with acute (<6 h) deep ganglionic ICH. Patients underwent CT scan at baseline and hematoma expansion (>33% or >12.5 ml increase) was determined on the second scan performed within 24 h. Fourteen clinical and neuroimaging variables (age, gender, GCS at admission, hypertension, diabetes mellitus, kidney disease, stroke, hemorrhagic, antiplatelet use, anticoagulant use, hematoma density heterogeneity, hematoma shape irregularity, hematoma volume and presence of IVH) were registered. Additionally, blood pressure was registered at initial systolic BP (i-SBP) and systolic BP 1.5 h after admission (1.5 h-SBP). The discriminant value of the hematoma volume and 1.5 h-SBP for hematoma expansion were determined by the receiver operating characteristic (ROC) curves. Factors associated with hematoma expansion were analyzed with multiple logistic regression.

Results

Early hematoma expansion occurred in 15 patients (7.0%). The cut-off value of hematoma volume and 1.5 h-SBP were determined to be 16 ml and 160 mmHg, respectively. Hematoma volume above 16 ml (HV > 16) ([OR] = 5.05, 95% CI 1.32–21.36, p = 0.018), hematoma heterogeneity (HH) ([OR] = 7.81, 95% CI 1.91–40.23, p = 0.004) and 1.5 h-SBP above 160 mmHg (1.5 h-SBP > 160) ([OR] = 8.77, 95% CI 2.33–44.56, p = 0.001) independently predicted ICH expansion. If those three factors were present, the probability was estimated to be 59%.

Conclusions

The presented model (HV > 16, HH, 1.5 h-SBP > 160) can be a practical tool for prediction of ICH growth in the acute stage. Further prospective studies are warranted to validate the ability of this model to predict clinical outcome.