Endoscopic resection as a first therapy for gastric epithelial atypia: is it reasonable?

BACKGROUND AND AIMS: Gastric atypical cell (GAC), an indefinite pathologic finding, often requires repeated biopsy or other diagnostic treatments, such as endoscopic mucosal resection (EMR), endoscopic submucosal dissection (ESD), or operation (OP). The aim of this study was to analyze the initial endoscopic and histologic findings of GAC and to discuss the necessity of EMR/ESD at establishing a correct diagnosis. METHODS: This retrospective study enrolled 96 patients proven as GAC on index forceps biopsy. ESD (17/96, 17.7%), EMR (5/96, 5.2%), OP (20/96, 20.8%), and other treatment or follow-up (54/96, 56.3%) were performed. We analyzed the initial endoscopic and histologic characteristics of GAC lesions, predictive of neoplasm. RESULTS: After diagnostic modalities, the final pathologic diagnoses were cancer (36/96, 37.6%), dysplasia (9/96, 9.4%), and non-neoplasm (51/96, 53.0%). In univariate analysis, age [odds ratio (OR) 1.04, 95% confidence interval (CI) 1.01-1.07], lesion size of 10 mm or greater (OR 3.94, 95% CI 1.61-9.61), lesion with depressed type (OR 2.50, 95% CI 1.09-5.72), and presence of H. pylori (OR 2.83, 95% CI 1.11-7.25) were risk factors for neoplasm. In multivariate analysis, lesion size of 10 mm or greater (OR 3.63, 95% CI 1.23-10.66), lesion with depressed type (OR 2.86, 95% CI 1.11-7.38) were independent risk factors for cancer. CONCLUSION: Considering the neoplastic risk of GAC, which could be missed on biopsy, more comprehensive tissue sampling via EMR/ESD might be necessary to establish a definite diagnosis.

A case of rapidly progressive IgA nephropathy in a patient with exacerbation of Crohn's disease.

BACKGROUND: IgA nephropathy has been reported as a renal involvement in Crohn's disease. Crescentic IgA nephropathy, which accounts for fewer than 5% of cases of IgA nephropathy, has a poorer prognosis than other forms of crescentic glomerulonephritis. We recently experienced a case of rapidly progressive IgA nephropathy concurrent with exacerbation of Crohn's disease. CASE PRESENTATION: An 18-year-old male diagnosed with Crohn's disease underwent a hemicolectomy 2 years prior previously. He had maintained a state of Crohn's disease remission with 5-aminosalicylic acid treatment. Four months prior to referral to the nephrology clinic, he experienced non-bloody diarrhea. He simultaneously developed proteinuria and microscopic hematuria with deterioration of renal function. Based on renal biopsy findings, the patient was diagnosed with crescentic IgA nephropathy. Immunostaining for interleukin-17 in renal tissue and previous exacerbated colonic ulcers was positive. Steroid pulse therapy was administered, followed by high-dose glucocorticoid and oral cyclophosphamide therapy. The patient's renal function recovered and his gastrointestinal symptoms were alleviated. CONCLUSIONS: We report a case of crescentic IgA nephropathy presenting with exacerbation of Crohn's disease, and present a review of the literature focusing on the pathophysiologic relationship between these two conditions.

A case of transient central diabetes insipidus after aorto-coronary bypass operation.

Diabetes insipidus (DI) is characterized by excessive urination and thirst. This disease results from inadequate output of antidiuretic hormone (ADH) from the pituitary gland or the absence of the normal response to ADH in the kidney. We present a case of transient central DI in a patient who underwent a cardiopulmonary bypass (CPB) for coronary artery bypass grafting (CABG). A 44-yr-old male underwent a CABG operation. An hour after the operation, the patient developed polyuria and was diagnosed with central DI. The patient responded to desmopressin and completely recovered five days after surgery. It is probable that transient cerebral ischemia resulted in the dysfunction of osmotic receptors in the hypothalamus or hypothalamus-pituitary axis during CPB. It is also possible that cardiac standstill altered the left atrial non-osmotic receptor function and suppressed ADH release. Therefore, we suggest that central DI is a possible cause of polyuria after CPB.

Plasma neutrophil gelatinase-associated lipocalin as a potential predictor of adverse renal outcomes in immunoglobulin A nephropathy.

BACKGROUND/AIMS: Neutrophil gelatinase-associated lipocalin (NGAL) is a well-known biomarker of acute kidney injury. We evaluated the value of plasma NGAL (pNGAL) as an independent predictor of prognosis in immunoglobulin A nephropathy (IgAN). METHODS: In total, 91 patients with biopsy-proven IgAN at a single center were evaluated. pNGAL was measured using a commercial enzyme-linked immunosorbent assay kit (R&D Systems). Adverse renal outcome was defined as chronic kidney disease (CKD) stage 3 or above at the last follow-up. Pearson correlation coefficient and Cox regression were used for analyses. RESULTS: The mean age of all patients (male:female, 48:43) was 35 years (range, 18 to 77). pNGAL ranged between 21.68 and 446.40 ng/mL (median, 123.97) and showed a correlation with age (r = 0.332, p = 0.001), creatinine (r = 0.336, p = 0.001), estimated glomerular filtration rate (r = -0.397, p < 0.001), uric acid (r = 0.289, p = 0.006), and the protein-to-creatinine ratio (r = 0.288, p = 0.006). During a mean follow-up period of 37.6 months, 11 patients (12.1%) had CKD stage 3 or above. In a multivariate Cox regression model, hypertension (hazard ratio [HR], 8.779; 95% confidence interval [CI], 1.526 to 50.496; p = 0.015), proteinuria > 1 g/day (HR, 5.184; 95% CI, 1.124 to 23.921; p = 0.035), and pNGAL (HR, 1.012; 95% CI, 1.003 to 1.022; p = 0.013) were independent predictors associated with adverse renal outcome. CONCLUSIONS: pNGAL showed strong correlations with other clinical prognostic factors and was also an independent predictor of adverse renal outcome. We suggest pNGAL as a potential predictor for prognosis in IgAN, while further studies are needed to confirm the clinical value.

Regression of Colonic Adenomas After Treatment With Sulindac in Familial Adenomatous Polyposis: A Case With a 2-Year Follow-up Without a Prophylactic Colectomy.

Familial adenomatous polyposis (FAP) is an autosomal dominant disorder characterized by hundreds of colorectal adenomatous polyps that progress to colorectal cancer. Management of patients with FAP is with a total colectomy. Chemopreventive strategies have been studied in FAP patients in an effort to delay the development of adenomas in the upper and the lower gastrointestinal tract and to prevent recurrence of adenomas in the retained rectum of patients after prophylactic surgery. Sulindac, a nonsteroidal anti-inflammatory drug, causes regression of colorectal adenomas in the retained rectal segment of FAP patients. However, evidence regarding long-term use of this therapy and its effect on the intact colon has been insufficient. We report a case in which the long-term use of sulindac was effective in reducing the size and the number of colonic polyps in patients with FAP without a prophylactic colectomy and polypectomy; we also present a review of the literature.

Impact of gene polymorphisms of interleukin-18, transforming growth factor-ß, and vascular endothelial growth factor on development of IgA nephropathy and thin glomerular basement membrane disease.

BACKGROUND: We investigated the effects of gene polymorphisms on the development of IgA nephropathy and thin glomerular basement membrane (GBM) disease by analyzing polymorphisms in the interleukin (IL)-18, transforming growth factor (TGF)-ß, and vascular endothelial growth factor (VEGF) genes in Korean patients. METHODS: This study included 146 normal individuals and 69 biopsy-proven IgA nephropathy and 44 thin GBM disease patients. The gene polymorphisms -607 A/C and -137 G/C in IL-18, -509C/T and T869C in TGF-ß, and -2578C/A and 405C/G in VEGF were investigated in DNA extracted from peripheral blood. RESULTS: The frequencies of the IL-18 -607CC genotype (43.5% vs. 21.2%, P=0.002, P corrected=0.012) and the VEGF 405 GG genotype (37.7% vs. 21.2%, P=0.002, P corrected=0.012) were significantly increased in the IgA nephropathy group compared with the control group, whereas no significant differences in genotype frequency were observed between the thin GBM disease and control groups. However, there were no significant differences in genotype and allele frequencies between the IgA nephropathy and thin GBM disease groups. CONCLUSION: This study did not show any statistically significant differences of six selected gene polymorphisms of the IL-18, TGF-ß, and VEGF genes between IgA nephropathy and thin GBM disease. Additional extensive studies are required to clarify the potential role of gene polymorphism to discriminate IgA nephropathy and thin GBM disease without renal biopsy.